Honglong Fang, Juan Chen, Jian Luo, Jianhua Hu, Danqiong Wang, L. Lv, Weiwen Zhang
Lung injury is one of the leading causes of death in sepsis. Abietic acid (AA) has demonstrated anti-inflammatory and bacteriostatic properties. Herein, we established a mouse model of sepsis by cecal ligation and puncture, and intraperitoneally injected AA to treat. Lung injury was assessed by H&E staining and the inflammation in bronchoalveolar lavage fluid (BALF) were assessed by counting the number of inflammatory cells and detecting the content of inflammatory factors. Meanwhile, we also designed to study the effect of AA on lipopolysaccharide (LPS)-induced inflammatory response and macrophage marker gene expression in RAW264.7 cells in vitro. In this study, we found that AA inhibited LPS-induced secretion of inflammatory mediators (IL-1β, TNF-α, IL-6 and MIP-2), and decreased the expression of M1 macrophage e markers (CD16 and iNOS) and p-p65 protein, while increased the expression of M2 macrophage markers (CD206 and Arg-1) in RAW264.7 cells in vitro. In vivo, the therapy of AA not only rescued septic animals, but also attenuated lung injury in sepsis mice. Moreover, AA decreased the number of total cells, neutrophils and macrophages, the conceration of total protein, and the levels of inflammatory mediators in BALF of sepsis mice. Further, we found that AA inhibited M1 macrophage polarization and blocked nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway in BALF of sepsis mice. In conclusion, Abietic acid attenuates sepsis-induced lung injury, and its mechanism may be related to reducing inflammation by inhibiting NF-κB signaling to inhibit M1 macrophage polarization.
{"title":"Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization","authors":"Honglong Fang, Juan Chen, Jian Luo, Jianhua Hu, Danqiong Wang, L. Lv, Weiwen Zhang","doi":"10.1538/expanim.22-0018","DOIUrl":"https://doi.org/10.1538/expanim.22-0018","url":null,"abstract":"Lung injury is one of the leading causes of death in sepsis. Abietic acid (AA) has demonstrated anti-inflammatory and bacteriostatic properties. Herein, we established a mouse model of sepsis by cecal ligation and puncture, and intraperitoneally injected AA to treat. Lung injury was assessed by H&E staining and the inflammation in bronchoalveolar lavage fluid (BALF) were assessed by counting the number of inflammatory cells and detecting the content of inflammatory factors. Meanwhile, we also designed to study the effect of AA on lipopolysaccharide (LPS)-induced inflammatory response and macrophage marker gene expression in RAW264.7 cells in vitro. In this study, we found that AA inhibited LPS-induced secretion of inflammatory mediators (IL-1β, TNF-α, IL-6 and MIP-2), and decreased the expression of M1 macrophage e markers (CD16 and iNOS) and p-p65 protein, while increased the expression of M2 macrophage markers (CD206 and Arg-1) in RAW264.7 cells in vitro. In vivo, the therapy of AA not only rescued septic animals, but also attenuated lung injury in sepsis mice. Moreover, AA decreased the number of total cells, neutrophils and macrophages, the conceration of total protein, and the levels of inflammatory mediators in BALF of sepsis mice. Further, we found that AA inhibited M1 macrophage polarization and blocked nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway in BALF of sepsis mice. In conclusion, Abietic acid attenuates sepsis-induced lung injury, and its mechanism may be related to reducing inflammation by inhibiting NF-κB signaling to inhibit M1 macrophage polarization.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"481 - 490"},"PeriodicalIF":0.0,"publicationDate":"2022-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42329096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nergis Akbaş, B. Suleyman, R. Mammadov, G. Yazici, S. Bulut, H. Süleyman
The role of oxidative stress and inflammation in the pathogenesis of cyclophosphamide-related side effects has been demonstrated in previous studies. This study aimed to investigate the effect of taxifolin, due to its antioxidant and anti-inflammatory properties, on cyclophosphamide-induced oxidative and inflammatory bladder injury in albino Wistar rats. The taxifolin+cyclophosphamide (TCYC) group was given 50 mg/kg of taxifolin orally by gavage. Normal saline was used as a solvent for the cyclophosphamide (CYC) group and the healthy control (HC) group. One hour after taxifolin administration, 75 mg/kg of cyclophosphamide was intraperitoneally injected in the TCYC and CYC groups. This procedure was repeated once a day for 30 days. At the end of this period, biochemical markers were studied in the excised bladder tissues and histopathological evaluations were conducted. In the histopathological evaluation of the CYC group, severe epithelial irregularity, dilatation, congestion, and polymorphonuclear leukocyte accumulation in the vascular structures were observed. Additionally, the malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels, the total oxidant status (TOS), and the oxidative stress index (OSI) values were significantly higher, and the total glutathione (tGSH) levels and total antioxidant status (TAS) were significantly lower in the CYC group in comparison to the HC group (P<0.001). Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-α, IL-1β, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001). Taxifolin may be useful in the treatment of cyclophosphamide-induced bladder damage.
{"title":"Effect of taxifolin on cyclophosphamide-induced oxidative and inflammatory bladder injury in rats","authors":"Nergis Akbaş, B. Suleyman, R. Mammadov, G. Yazici, S. Bulut, H. Süleyman","doi":"10.1538/expanim.22-0030","DOIUrl":"https://doi.org/10.1538/expanim.22-0030","url":null,"abstract":"The role of oxidative stress and inflammation in the pathogenesis of cyclophosphamide-related side effects has been demonstrated in previous studies. This study aimed to investigate the effect of taxifolin, due to its antioxidant and anti-inflammatory properties, on cyclophosphamide-induced oxidative and inflammatory bladder injury in albino Wistar rats. The taxifolin+cyclophosphamide (TCYC) group was given 50 mg/kg of taxifolin orally by gavage. Normal saline was used as a solvent for the cyclophosphamide (CYC) group and the healthy control (HC) group. One hour after taxifolin administration, 75 mg/kg of cyclophosphamide was intraperitoneally injected in the TCYC and CYC groups. This procedure was repeated once a day for 30 days. At the end of this period, biochemical markers were studied in the excised bladder tissues and histopathological evaluations were conducted. In the histopathological evaluation of the CYC group, severe epithelial irregularity, dilatation, congestion, and polymorphonuclear leukocyte accumulation in the vascular structures were observed. Additionally, the malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels, the total oxidant status (TOS), and the oxidative stress index (OSI) values were significantly higher, and the total glutathione (tGSH) levels and total antioxidant status (TAS) were significantly lower in the CYC group in comparison to the HC group (P<0.001). Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-α, IL-1β, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001). Taxifolin may be useful in the treatment of cyclophosphamide-induced bladder damage.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"460 - 467"},"PeriodicalIF":0.0,"publicationDate":"2022-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43043106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y. Ueda, Kentarou Suzuki, Mizuki Kajimoto, Kota Fujimoto, M. Mahendroo, M. Ema, G. Yamada, I. Hara
The development of embryonic external genitalia (eExG) into characteristic male structures, such as urethra and penile erectile tissues, depends on 5α-dihydrotestosterone (DHT). Although the corpus cavernosum (CC) is well known as essential for erectile function in adults, its developmental process and its dependency on DHT have been unknown. To reveal the dimorphic formation of the murine CC from the embryonic stage, we first analyzed the production of the protein vascular endothelial growth factor receptor-2 (FLK1) via its expression (hereinafter referred as “expression of FLK1”) and the expression of alpha-smooth muscle actin (ACTA2) and collagen type 1 (COL1A1) in developing external genitalia. The 5-α reductase type 2 encoded by the SRD5A2 gene has been suggested to be a crucial enzyme for male sexual differentiation, as it converts testosterone (T) into DHT in the local urogenital organs. In fact, SRD5A2 mutation results in decreased synthesis of DHT, which leads to various degrees of masculinized human external genitalia (ExG). We further investigated the expression profile of SRD5A2 during the formation of the murine CC. We observed that SRD5A2 was expressed in smooth muscle of the CC. To determine the role of SRD5A2 in CC formation, we analyzed the formation of erectile tissue in the male Srd5a2 KO mice and measured the levels of androgens in the ExG by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Intriguingly, there were no obvious defects in the CCs of male Srd5a2 KO mice, possibly due to increased T levels. The current study suggests possible redundant functions of androgens in CC development.
{"title":"Possible testosterone redundancy for 5α-dihydrotestosterone in the masculinization of mouse external genitalia","authors":"Y. Ueda, Kentarou Suzuki, Mizuki Kajimoto, Kota Fujimoto, M. Mahendroo, M. Ema, G. Yamada, I. Hara","doi":"10.1538/expanim.22-0038","DOIUrl":"https://doi.org/10.1538/expanim.22-0038","url":null,"abstract":"The development of embryonic external genitalia (eExG) into characteristic male structures, such as urethra and penile erectile tissues, depends on 5α-dihydrotestosterone (DHT). Although the corpus cavernosum (CC) is well known as essential for erectile function in adults, its developmental process and its dependency on DHT have been unknown. To reveal the dimorphic formation of the murine CC from the embryonic stage, we first analyzed the production of the protein vascular endothelial growth factor receptor-2 (FLK1) via its expression (hereinafter referred as “expression of FLK1”) and the expression of alpha-smooth muscle actin (ACTA2) and collagen type 1 (COL1A1) in developing external genitalia. The 5-α reductase type 2 encoded by the SRD5A2 gene has been suggested to be a crucial enzyme for male sexual differentiation, as it converts testosterone (T) into DHT in the local urogenital organs. In fact, SRD5A2 mutation results in decreased synthesis of DHT, which leads to various degrees of masculinized human external genitalia (ExG). We further investigated the expression profile of SRD5A2 during the formation of the murine CC. We observed that SRD5A2 was expressed in smooth muscle of the CC. To determine the role of SRD5A2 in CC formation, we analyzed the formation of erectile tissue in the male Srd5a2 KO mice and measured the levels of androgens in the ExG by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Intriguingly, there were no obvious defects in the CCs of male Srd5a2 KO mice, possibly due to increased T levels. The current study suggests possible redundant functions of androgens in CC development.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"451 - 459"},"PeriodicalIF":0.0,"publicationDate":"2022-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42236291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We previously showed that a diet containing calcium carbonate causes impairments in spatial and recognition memory in mice. In this study, we investigated the effects of calcium carbonate supplementation on motor function. Motor function was determined using different tests that have been used to analyze different aspects of Parkinsonism. A catalepsy test for akinesia; a muscular strength assessment, pole test, beam-walking test, and gait analysis for motor coordination and balance assessment; and an open-field test for locomotor activity assessment were performed. The mice were fed diets containing 0.6% or 1.0% calcium carbonate for eight weeks, after which they were evaluated for motor functions. The diets containing calcium carbonate caused significant motor dysfunction, as revealed by the different tests, although the spontaneous locomotor activity did not change. Calcium carbonate supplementation decreased the dopamine content in the basal ganglia, including the striatum and substantia nigra, and the number of tyrosine hydroxylase-positive neurons in the substantia nigra. In addition, administration of L-dopa led to at least a partial recovery of motor dysfunction, suggesting that calcium carbonate supplementation causes motor dysfunction by decreasing the dopamine content in the basal ganglia. These results suggest that mice with calcium carbonate-induced motor dysfunction may be useful as a new animal model for Parkinson’s disease and Huntington’s disease.
{"title":"Calcium carbonate supplementation causes motor dysfunction","authors":"Ami Sugiura, Misaki Kitamura, Y. Hasegawa","doi":"10.1538/expanim.22-0011","DOIUrl":"https://doi.org/10.1538/expanim.22-0011","url":null,"abstract":"We previously showed that a diet containing calcium carbonate causes impairments in spatial and recognition memory in mice. In this study, we investigated the effects of calcium carbonate supplementation on motor function. Motor function was determined using different tests that have been used to analyze different aspects of Parkinsonism. A catalepsy test for akinesia; a muscular strength assessment, pole test, beam-walking test, and gait analysis for motor coordination and balance assessment; and an open-field test for locomotor activity assessment were performed. The mice were fed diets containing 0.6% or 1.0% calcium carbonate for eight weeks, after which they were evaluated for motor functions. The diets containing calcium carbonate caused significant motor dysfunction, as revealed by the different tests, although the spontaneous locomotor activity did not change. Calcium carbonate supplementation decreased the dopamine content in the basal ganglia, including the striatum and substantia nigra, and the number of tyrosine hydroxylase-positive neurons in the substantia nigra. In addition, administration of L-dopa led to at least a partial recovery of motor dysfunction, suggesting that calcium carbonate supplementation causes motor dysfunction by decreasing the dopamine content in the basal ganglia. These results suggest that mice with calcium carbonate-induced motor dysfunction may be useful as a new animal model for Parkinson’s disease and Huntington’s disease.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"399 - 410"},"PeriodicalIF":0.0,"publicationDate":"2022-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47468083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rufeng Zhang, Jing Zhang, Xiaofei Zhou, Ang Zhao, Changyuan Yu
In the field of cancer immunotherapy, monoclonal antibody drugs, bispecific antibodies, and antibody-conjugated drugs have become the focus of current research, and gene-edited animal models play an essential role in the entire drug development process. In this study, CD3E humanized mice were established by replacing the second to the seventh exon of the Cd3e mouse gene with the same exon of the human gene. The expression of human CD3E in CD3E humanized mice was detected by RT-PCR as well as flow cytometry, also a tumor model was established based on CD3E humanized mice, and the pharmacodynamic effects of CD3E monoclonal antibodies were evaluated. The results showed that CD3E humanized mice expressed only human CD3E, and the proportion of each lymphocyte in the thymus and spleen was not significantly changed compared with wild-type mice. CD3E monoclonal antibody could promote tumor growth after treatment, which may be related to the activation-induced cell death effect caused by this CD3E antibody. In contrast, Bispecific antibody blinatumomab inhibited tumor growth significantly. Thus, the CD3E humanized mice provided an adequate animal model for evaluating the efficacy and safety of CD3E antibody drugs.
{"title":"The establishment and application of CD3E humanized mice in immunotherapy","authors":"Rufeng Zhang, Jing Zhang, Xiaofei Zhou, Ang Zhao, Changyuan Yu","doi":"10.1538/expanim.22-0012","DOIUrl":"https://doi.org/10.1538/expanim.22-0012","url":null,"abstract":"In the field of cancer immunotherapy, monoclonal antibody drugs, bispecific antibodies, and antibody-conjugated drugs have become the focus of current research, and gene-edited animal models play an essential role in the entire drug development process. In this study, CD3E humanized mice were established by replacing the second to the seventh exon of the Cd3e mouse gene with the same exon of the human gene. The expression of human CD3E in CD3E humanized mice was detected by RT-PCR as well as flow cytometry, also a tumor model was established based on CD3E humanized mice, and the pharmacodynamic effects of CD3E monoclonal antibodies were evaluated. The results showed that CD3E humanized mice expressed only human CD3E, and the proportion of each lymphocyte in the thymus and spleen was not significantly changed compared with wild-type mice. CD3E monoclonal antibody could promote tumor growth after treatment, which may be related to the activation-induced cell death effect caused by this CD3E antibody. In contrast, Bispecific antibody blinatumomab inhibited tumor growth significantly. Thus, the CD3E humanized mice provided an adequate animal model for evaluating the efficacy and safety of CD3E antibody drugs.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"442 - 450"},"PeriodicalIF":0.0,"publicationDate":"2022-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45302272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study aimed to develop a more suitable ovarian stimulation procedure for cynomolgus macaques (Macaca fascicularis). Macaques were divided into 4 groups, 7AG, 8AG, 7AN, and 8AN, according to the ovarian stimulation procedure administered (i.e., administration of either a gonadotropin-releasing hormone agonist [GnRH-a] or GnRH antagonist [GnRH-ant]) and the number of menstruations (≤ 7 times or ≥ 8 times) in the previous year. In both procedures, oocyte growth and maturation were induced by administration of human follicle-stimulating hormone and human chorionic gonadotropin. The mean numbers of metaphase II mature and metaphase I premature oocytes collected from the 7AG, 8AG, 7AN, and 8AN groups were 12.1 and 10.4, 12.0 and 13.8, 9.1 and 8.3, and 15.5 and 8.8, respectively (P>0.05). The fertilization rates of the 7AN and 8AN groups (85.3% and 74.7%) tended to be higher compared with those in the 7AG and 8AG groups (59.1% and 47.3%; P>0.05). The 8AN group yielded 19.9 zygotes, which was the largest number per macaque, compared with the other three groups. Furthermore, regarding the decreases in body weight between the start of the procedures and the time of oocyte collection, those of the 7AN and 8AN groups were significantly smaller than those of the 7AG and 8AG groups (P<0.05), suggesting that the procedure involving GnRH-ant reduced the burden on the macaques. Thus, controlled ovarian stimulation using a GnRH-ant has some advantages for cynomolgus macaques compared with that using a GnRH-a.
{"title":"A controlled ovarian stimulation procedure suitable for cynomolgus macaques","authors":"N. Shimozawa, T. Iwata, Y. Yasutomi","doi":"10.1538/expanim.21-0198","DOIUrl":"https://doi.org/10.1538/expanim.21-0198","url":null,"abstract":"This study aimed to develop a more suitable ovarian stimulation procedure for cynomolgus macaques (Macaca fascicularis). Macaques were divided into 4 groups, 7AG, 8AG, 7AN, and 8AN, according to the ovarian stimulation procedure administered (i.e., administration of either a gonadotropin-releasing hormone agonist [GnRH-a] or GnRH antagonist [GnRH-ant]) and the number of menstruations (≤ 7 times or ≥ 8 times) in the previous year. In both procedures, oocyte growth and maturation were induced by administration of human follicle-stimulating hormone and human chorionic gonadotropin. The mean numbers of metaphase II mature and metaphase I premature oocytes collected from the 7AG, 8AG, 7AN, and 8AN groups were 12.1 and 10.4, 12.0 and 13.8, 9.1 and 8.3, and 15.5 and 8.8, respectively (P>0.05). The fertilization rates of the 7AN and 8AN groups (85.3% and 74.7%) tended to be higher compared with those in the 7AG and 8AG groups (59.1% and 47.3%; P>0.05). The 8AN group yielded 19.9 zygotes, which was the largest number per macaque, compared with the other three groups. Furthermore, regarding the decreases in body weight between the start of the procedures and the time of oocyte collection, those of the 7AN and 8AN groups were significantly smaller than those of the 7AG and 8AG groups (P<0.05), suggesting that the procedure involving GnRH-ant reduced the burden on the macaques. Thus, controlled ovarian stimulation using a GnRH-ant has some advantages for cynomolgus macaques compared with that using a GnRH-a.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"426 - 432"},"PeriodicalIF":0.0,"publicationDate":"2022-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46797632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F. Duparc, M. Noyon, J. Ozeel, A. Gerometta, C. Michot, M. Tadjalli, H. Moslemy, S. Safaei, A. Heiman, S. Wish-Baratz, T. Melnikov, E. Smoliar, A. Håkan, F. Yucel, D. Kachlík, M. Pešl, V. Baca, J. Stingl, K. D. Kachlík, C. Cech, B. Baca, B. Mompeó, A. Marrero-Rodriguez, A. Zeybek, B. Sağlam, E. Çikler, Ş. Çetinel, F. Ercan, G. Şener, Y. Kawawa, E. Kohda, T. Tatsuya, M. Moroi, T. Kunimasa, M. Nagamoto, H. Terada, B. Labuschagne, T. J. Krieke, P. Hoogland, C. Muller, R. Lyners, W. Vorster, P. Matusz, D. E. Zaboi, S. C. Xu, L. Tu, Q. Wang, M. Zhang, H. Han, W. Tao, Y. Jiao, G. Pang, M. Aydın, C. Kopuz, M. Demir, M. Yıldırım, A. Kale, Y. Ince, K. Khamanarong, P. Jeeravipoolvarn, W. Chaijaroonkhanarak, W. Gawgleun, T. Fujino, A. Uz, N. Apaydın, M. Bozkurt, A. Elhan, M. Sheibani, M. Adibmoradi, N. Jahovic, I. Alican, G. Erkanlı, S. Arbak, S. Karakas, F. Taser, H. Güneş, Y. Yildiz, Y. Yazıcı, R. Aland, V. Kippers, W. Song, S. Park, C. Shin, K. Koh, G. Russo, F. Pomara, M. Veca, F. Cacciola, U. Martorana, G. Grav
{"title":"Poster Presentation","authors":"F. Duparc, M. Noyon, J. Ozeel, A. Gerometta, C. Michot, M. Tadjalli, H. Moslemy, S. Safaei, A. Heiman, S. Wish-Baratz, T. Melnikov, E. Smoliar, A. Håkan, F. Yucel, D. Kachlík, M. Pešl, V. Baca, J. Stingl, K. D. Kachlík, C. Cech, B. Baca, B. Mompeó, A. Marrero-Rodriguez, A. Zeybek, B. Sağlam, E. Çikler, Ş. Çetinel, F. Ercan, G. Şener, Y. Kawawa, E. Kohda, T. Tatsuya, M. Moroi, T. Kunimasa, M. Nagamoto, H. Terada, B. Labuschagne, T. J. Krieke, P. Hoogland, C. Muller, R. Lyners, W. Vorster, P. Matusz, D. E. Zaboi, S. C. Xu, L. Tu, Q. Wang, M. Zhang, H. Han, W. Tao, Y. Jiao, G. Pang, M. Aydın, C. Kopuz, M. Demir, M. Yıldırım, A. Kale, Y. Ince, K. Khamanarong, P. Jeeravipoolvarn, W. Chaijaroonkhanarak, W. Gawgleun, T. Fujino, A. Uz, N. Apaydın, M. Bozkurt, A. Elhan, M. Sheibani, M. Adibmoradi, N. Jahovic, I. Alican, G. Erkanlı, S. Arbak, S. Karakas, F. Taser, H. Güneş, Y. Yildiz, Y. Yazıcı, R. Aland, V. Kippers, W. Song, S. Park, C. Shin, K. Koh, G. Russo, F. Pomara, M. Veca, F. Cacciola, U. Martorana, G. Grav","doi":"10.1007/BF03371476","DOIUrl":"https://doi.org/10.1007/BF03371476","url":null,"abstract":"","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"S77 - S173"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03371476","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48923720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myocardial infarction (MI) as the remarkable presentation of coronary artery disease is still a reason for morbidity and mortality in worldwide. Lysosomal-associated protein transmembrane 5 (LAPTM5) is a lysosomal-related protein found in hematopoietic tissues and has been confirmed as a positive regulator of pro-inflammatory pathways in macrophages. However, the role of LAPTM5 in MI remains unknown. In this study, we found that both mRNA and protein expression levels of LAPTM5 were significantly elevated in MI mice. Suppression of LAPTM5 in myocardial tissues decreased cardiac fibrosis and improved cardiac function after MI. At the molecular level, downregulated LAPTM5 dramatically suppressed the macrophage activation and inflammatory response via inhibiting the activation of the nuclear factor-kappa B (NF-κB) pathway. Collectively, suppression of LAPTM5 in myocardial tissues inhibits the pro-inflammatory response and the cardiac dysfunction caused by MI. This study indicated that LAPTM5 as a pro-inflammatory factor plays a crucial role in MI disease.
{"title":"Suppression of lysosomal-associated protein transmembrane 5 ameliorates cardiac function and inflammatory response by inhibiting the nuclear factor-kappa B (NF-κB) pathway after myocardial infarction in mice","authors":"Zhanchun Song, Xiaozeng Wang, Lianqi He, Liang Chen, Zhi-Juan Ren, Siyu Song","doi":"10.1538/expanim.22-0008","DOIUrl":"https://doi.org/10.1538/expanim.22-0008","url":null,"abstract":"Myocardial infarction (MI) as the remarkable presentation of coronary artery disease is still a reason for morbidity and mortality in worldwide. Lysosomal-associated protein transmembrane 5 (LAPTM5) is a lysosomal-related protein found in hematopoietic tissues and has been confirmed as a positive regulator of pro-inflammatory pathways in macrophages. However, the role of LAPTM5 in MI remains unknown. In this study, we found that both mRNA and protein expression levels of LAPTM5 were significantly elevated in MI mice. Suppression of LAPTM5 in myocardial tissues decreased cardiac fibrosis and improved cardiac function after MI. At the molecular level, downregulated LAPTM5 dramatically suppressed the macrophage activation and inflammatory response via inhibiting the activation of the nuclear factor-kappa B (NF-κB) pathway. Collectively, suppression of LAPTM5 in myocardial tissues inhibits the pro-inflammatory response and the cardiac dysfunction caused by MI. This study indicated that LAPTM5 as a pro-inflammatory factor plays a crucial role in MI disease.","PeriodicalId":75961,"journal":{"name":"Jikken dobutsu. Experimental animals","volume":"71 1","pages":"415 - 425"},"PeriodicalIF":0.0,"publicationDate":"2022-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42409823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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