{"title":"Anti-Inflammatory Effects of Chaenomeles sinensis Extract in an ALS Animal Model","authors":"Eun Jin Yang, Sun Hwa Lee","doi":"10.31083/j.fbl2812326","DOIUrl":"https://doi.org/10.31083/j.fbl2812326","url":null,"abstract":"","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138619185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective : The use of immune checkpoint inhibitors (ICIs) provides promising strategies for hepatocellular carcinoma (HCC) treat-ment. This study aimed to explore impact and underlying mechanism of the combination therapy of quercetin and anti-programmed cell death 1 (anti-PD-1) antibody on HCC. Methods : Orthotopically transplanted HCC tumors in mice were treated with quercetin, anti-PD-1 antibody
{"title":"Quercetin/Anti-PD-1 Antibody Combination Therapy Regulates the Gut Microbiota, Impacts Macrophage Immunity and Reshapes the Hepatocellular Carcinoma Tumor Microenvironment","authors":"Ruoxia Wu, Jiaqing Xiong, Ting Zhou, Zhen Zhang, Zhen Huang, Sha Tian, Yongli Wang","doi":"10.31083/j.fbl2812327","DOIUrl":"https://doi.org/10.31083/j.fbl2812327","url":null,"abstract":"Objective : The use of immune checkpoint inhibitors (ICIs) provides promising strategies for hepatocellular carcinoma (HCC) treat-ment. This study aimed to explore impact and underlying mechanism of the combination therapy of quercetin and anti-programmed cell death 1 (anti-PD-1) antibody on HCC. Methods : Orthotopically transplanted HCC tumors in mice were treated with quercetin, anti-PD-1 antibody","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"101 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138608902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background : Dexmedetomidine (DEX) reportedly protects against ischemia-reperfusion (I/R) injury and associated damage to the kidneys, but the underlying mechanisms have yet to be established. Methods : Unilateral nephrectomy was performed in Wistar rats, and the remaining kidney was clamped for 1 h prior to reperfusion to establish an experimental model system. These animals were then randomized into Sham, DEX + Sham, DEX + I/R, ATI (Altepamizole, α 2-adrenergic receptor inhibitor) + DEX + I/R, and 3-MA (3-methyladenine, autophagy inhibitor) + DEX + I/R groups. Serum renal function biomarkers, acute kidney injury (AKI) histopathological scores, serum inflammatory factors, redox biomarkers, markers of autophagic flux, and autophagosome numbers were assessed. Levels of proteins related to the autophagic pathway, including mTOR and AMPK, were also analyzed. Results : Serum creatinine and urea nitrogen levels in the I/R group were significantly elevated over those in sham control rats, as were AKI scores, serum inflammatory cytokine concentrations (IL-6, IL-1 β , and TNF-α ), and serum levels of the oxidative stress biomarker malondialdehyde (MDA). All of these parameters were significantly reduced in the DEX + I/R group relative to I/R model rats. I/R group rats also exhibited significant decreases in renal levels of autophagic flux-related biomarkers and autophagosome numbers relative to sham controls, while DEX administration partially restored normal autophagic flux in these rats. Acute I/R also suppress the expression of AMPK in the kidney while increasing mTOR expression, and DEX reversed these effects. The beneficial impact of DEX on I/R-associated AKI was ablated by ATI or 3-MA administration. Conclusions : These analyses provide strong evidence for the ability of DEX to protect against I/R-associated AKI via the α 2-AR/AMPK/mTOR pathway-mediated enhancement of autophagic activity.
{"title":"Dexmedetomidine Alleviates Ischemia/Reperfusion-Associated Acute Kidney Injury by Enhancing Autophagic Activity via the α2-AR/AMPK/mTOR Pathway","authors":"Bi-Ying Zhou, Jing Yang, Rui-Rui Luo, Yan-Lin Sun, Hao-Tian Zhang, Ai-Xiang Yang, Guo-Xing Zhang","doi":"10.31083/j.fbl2812323","DOIUrl":"https://doi.org/10.31083/j.fbl2812323","url":null,"abstract":"Background : Dexmedetomidine (DEX) reportedly protects against ischemia-reperfusion (I/R) injury and associated damage to the kidneys, but the underlying mechanisms have yet to be established. Methods : Unilateral nephrectomy was performed in Wistar rats, and the remaining kidney was clamped for 1 h prior to reperfusion to establish an experimental model system. These animals were then randomized into Sham, DEX + Sham, DEX + I/R, ATI (Altepamizole, α 2-adrenergic receptor inhibitor) + DEX + I/R, and 3-MA (3-methyladenine, autophagy inhibitor) + DEX + I/R groups. Serum renal function biomarkers, acute kidney injury (AKI) histopathological scores, serum inflammatory factors, redox biomarkers, markers of autophagic flux, and autophagosome numbers were assessed. Levels of proteins related to the autophagic pathway, including mTOR and AMPK, were also analyzed. Results : Serum creatinine and urea nitrogen levels in the I/R group were significantly elevated over those in sham control rats, as were AKI scores, serum inflammatory cytokine concentrations (IL-6, IL-1 β , and TNF-α ), and serum levels of the oxidative stress biomarker malondialdehyde (MDA). All of these parameters were significantly reduced in the DEX + I/R group relative to I/R model rats. I/R group rats also exhibited significant decreases in renal levels of autophagic flux-related biomarkers and autophagosome numbers relative to sham controls, while DEX administration partially restored normal autophagic flux in these rats. Acute I/R also suppress the expression of AMPK in the kidney while increasing mTOR expression, and DEX reversed these effects. The beneficial impact of DEX on I/R-associated AKI was ablated by ATI or 3-MA administration. Conclusions : These analyses provide strong evidence for the ability of DEX to protect against I/R-associated AKI via the α 2-AR/AMPK/mTOR pathway-mediated enhancement of autophagic activity.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"111 13","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138609601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background : Delayed wound healing, a common problem in patients with diabetes mellitus (DM), is associated with impaired keratinocyte autophagy. Epigallocatechin gallate (EGCG), a catechin, has been proven to promote diabetic wound healing. This study aims to explore the therapeutic mechanism of EGCG on diabetic wound healing. Methods : High glucose (HG)-induced keratinocytes and streptozotocin (STZ)-induced DM rats were prepared and intervened with EGCG to examine its therapeutic effects in in vivo and in vitro settings. The AMPK inhibitor, Compound C, was utilized to determine whether EGCG exerted its therapeutic effects through the AMPK/ULK1 pathway. Results : In vitro , EGCG improved HG-induced autophagy impairment in keratinocytes by increasing LC3II/LC3I, Becline1, and ATG5 levels and decreasing p62 level. Mechanically, EGCG activated the AMPK/ULK1 pathway, thereby promoting keratinocyte autophagy through the phosphorylation of AMPK and ULK1. Notably, EGCG promoted the proliferation, migration, synthesis and release of C-C motif chemokine ligand 2 (CCL2) in HG-treated keratinocytes. Furthermore, EGCG indirectly promoted the activation of fibroblasts, as evidenced by increased alpha-smooth muscle actin ( α -SMA) and Collagen I levels. In vivo , EGCG promoted wound healing in DM rats, primarily by reducing inflammatory infiltration and increasing granulation tissue to promote wound epithelialization. Besides, EGCG promoted ATG5, KRT10, KRT14, TGF-β 1, Collagen I, and α -SMA expressions in the neonatal epithelial tissues of DM rats. However, the use of Compound C reversed the effects of EGCG. Conclusions : These findings indicated that EGCG restored keratinocyte autophagy to promote diabetic wound healing through the AMPK/ULK1 pathway.
{"title":"EGCG Restores Keratinocyte Autophagy to Promote Diabetic Wound Healing through the AMPK/ULK1 Pathway","authors":"Chao Tian, Yuchao Feng, Tianhua Chen, Zuyang Zhang, Xiaojie He, Liangdong Jiang, Mingjiang Liu","doi":"10.31083/j.fbl2812324","DOIUrl":"https://doi.org/10.31083/j.fbl2812324","url":null,"abstract":"Background : Delayed wound healing, a common problem in patients with diabetes mellitus (DM), is associated with impaired keratinocyte autophagy. Epigallocatechin gallate (EGCG), a catechin, has been proven to promote diabetic wound healing. This study aims to explore the therapeutic mechanism of EGCG on diabetic wound healing. Methods : High glucose (HG)-induced keratinocytes and streptozotocin (STZ)-induced DM rats were prepared and intervened with EGCG to examine its therapeutic effects in in vivo and in vitro settings. The AMPK inhibitor, Compound C, was utilized to determine whether EGCG exerted its therapeutic effects through the AMPK/ULK1 pathway. Results : In vitro , EGCG improved HG-induced autophagy impairment in keratinocytes by increasing LC3II/LC3I, Becline1, and ATG5 levels and decreasing p62 level. Mechanically, EGCG activated the AMPK/ULK1 pathway, thereby promoting keratinocyte autophagy through the phosphorylation of AMPK and ULK1. Notably, EGCG promoted the proliferation, migration, synthesis and release of C-C motif chemokine ligand 2 (CCL2) in HG-treated keratinocytes. Furthermore, EGCG indirectly promoted the activation of fibroblasts, as evidenced by increased alpha-smooth muscle actin ( α -SMA) and Collagen I levels. In vivo , EGCG promoted wound healing in DM rats, primarily by reducing inflammatory infiltration and increasing granulation tissue to promote wound epithelialization. Besides, EGCG promoted ATG5, KRT10, KRT14, TGF-β 1, Collagen I, and α -SMA expressions in the neonatal epithelial tissues of DM rats. However, the use of Compound C reversed the effects of EGCG. Conclusions : These findings indicated that EGCG restored keratinocyte autophagy to promote diabetic wound healing through the AMPK/ULK1 pathway.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jianan Sui, Jiazi Chen, Yuehui Chen, Naoki Iwamori, Jin Sun
{"title":"ProSE-Pero: Peroxisomal Protein Localization Identification Model Based on Self-Supervised Multi-Task Language Pre-Training Model","authors":"Jianan Sui, Jiazi Chen, Yuehui Chen, Naoki Iwamori, Jin Sun","doi":"10.31083/j.fbl2812322","DOIUrl":"https://doi.org/10.31083/j.fbl2812322","url":null,"abstract":"","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"14 22","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138624916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Na Yao, B-B Guo, Yuhang Wang, Ying Hu, Xiao-fang Zhu, Jiaxin Cao, Yi Liu, Y. Qian, Hua Sang, Wei-Wei Zhu
BACKGROUND Circulating levels of arginine vasopressin (AVP) are elevated during cardiac stress and this could be a factor in cardiac inflammation and fibrosis. Herein, we studied the effects of AVP on interleukin-1β (IL-1β) production and the role(s) of β-arrestin2-dependent signaling in murine heart. METHODS The levels of IL-1β mRNA and protein in adult rat cardiofibroblasts (ARCFs) was measured using quantitative PCR and ELISA, respectively. The activity of β-arrestin2 was manipulated using either pharmacologic inhibitors or through recombinant β-arrestin2 over-expression. These experiments were conducted to determine the roles of β-arrestin2 in the regulation of AVP-induced IL-1β and NLRP3 inflammasome production. The phosphorylation and activation of NF-κB induced by AVP was measured by immunoblotting. β-arrestin2 knockout (KO) mice were used to investigate whether β-arrestin2 mediated the AVP-induced production of IL-1β and NLRP3, as well as the phosphorylation of the NF-κB p65 subunitin mouse myocardium. Prism GraphPad software(version 8.0), was used for all statistical analyses. RESULTS AVP induced the expression of IL-1β in a time-dependent manner in ARCFs but not in cultured adult rat cardiomyocytes (ARCMs). The inhibition of NF-κB with pyrrolidinedithiocarbamic acid (PDTC) prevented the AVP-induced phosphorylation of NF-κB and production of IL-1β and NLRP3 in ARCFs. The deletion of β-arrestin2 blocked the phosphorylation of p65 and the expression of NLRP3 and IL-1β induced by AVP in both mouse hearts and in ARCFs. CONCLUSIONS AVP promotes IL-1β expression through β-arrestin2-mediated NF-κB signaling in murine heart.
{"title":"β-arrestin2 Mediates the Arginine Vasopressin-Induced Expression of IL-1β in Murine Hearts.","authors":"Na Yao, B-B Guo, Yuhang Wang, Ying Hu, Xiao-fang Zhu, Jiaxin Cao, Yi Liu, Y. Qian, Hua Sang, Wei-Wei Zhu","doi":"10.31083/j.fbl2712350","DOIUrl":"https://doi.org/10.31083/j.fbl2712350","url":null,"abstract":"BACKGROUND\u0000Circulating levels of arginine vasopressin (AVP) are elevated during cardiac stress and this could be a factor in cardiac inflammation and fibrosis. Herein, we studied the effects of AVP on interleukin-1β (IL-1β) production and the role(s) of β-arrestin2-dependent signaling in murine heart.\u0000\u0000\u0000METHODS\u0000The levels of IL-1β mRNA and protein in adult rat cardiofibroblasts (ARCFs) was measured using quantitative PCR and ELISA, respectively. The activity of β-arrestin2 was manipulated using either pharmacologic inhibitors or through recombinant β-arrestin2 over-expression. These experiments were conducted to determine the roles of β-arrestin2 in the regulation of AVP-induced IL-1β and NLRP3 inflammasome production. The phosphorylation and activation of NF-κB induced by AVP was measured by immunoblotting. β-arrestin2 knockout (KO) mice were used to investigate whether β-arrestin2 mediated the AVP-induced production of IL-1β and NLRP3, as well as the phosphorylation of the NF-κB p65 subunitin mouse myocardium. Prism GraphPad software(version 8.0), was used for all statistical analyses.\u0000\u0000\u0000RESULTS\u0000AVP induced the expression of IL-1β in a time-dependent manner in ARCFs but not in cultured adult rat cardiomyocytes (ARCMs). The inhibition of NF-κB with pyrrolidinedithiocarbamic acid (PDTC) prevented the AVP-induced phosphorylation of NF-κB and production of IL-1β and NLRP3 in ARCFs. The deletion of β-arrestin2 blocked the phosphorylation of p65 and the expression of NLRP3 and IL-1β induced by AVP in both mouse hearts and in ARCFs.\u0000\u0000\u0000CONCLUSIONS\u0000AVP promotes IL-1β expression through β-arrestin2-mediated NF-κB signaling in murine heart.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"3 1","pages":"7"},"PeriodicalIF":3.1,"publicationDate":"2022-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73683834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Moncayo-Estrada, J. Cruz-Agüero, E. López-López, P. Monte-Luna, María Magdalena Díaz-Argüero, Arturo Chacón-Torres, A. Ramírez-García, O. Domínguez‐Domínguez, J. P. Ramírez-Herrejón
BACKGROUND Analyses of spatial and temporal patterns and interactions are important for determining the abiotic factors limiting populations and the impact from other species and different anthropogenic stressors that promote the extirpation of species. The fish Hubbsina turneri de Buen (1940) was studied as a model species in a historical context at varying locations. Originally distributed only in the Lerma-Chapala basin, the main lake complex in Mexico, this species has not been collected from Lake Cuitzeo (LC) and now is restricted to Lake Zacapu (LZ). At present, the Highland splitfin is classified as critically endangered. METHODS Historical information of LC and historical and current information from LZ were explored by applying cluster analysis and generalized additive mixed model (GAMM) to describe the biotic interactions among fish species and the relationship between density and environmental variables, respectively. The two lakes' contrasting abiotic/biotic characteristics provided elements to describe some species distribution limits in chemical ion gradients. Extirpation calendar dates were estimated using an optimal linear estimation method. Finally, a bibliographic review was conducted on the causes that promoted the extirpation and restriction of H. turneri and the prognosis for its reestablishment and conservation. RESULTS Clusters showed the fishes relationship according to their distribution along the lakes. GAMM indicated that high H. turneri density is related to low hardness/fecal coliforms, medium depth/suspended solids, and high oxygen concentration. Estimated extirpation dates were between the years 2013 and 2018. The extirpation was linked to an abrupt drop in the LC volume, water quality degradation, increased biotic interactions within macrophytes habitats with native and introduced species, and fisheries bycatches. The current restricted range of H. turneri resulted from the draining of the larger lake, forcing the remaining populations to small spring-fed remnants. Recent samplings in LZ resulted in a low number of individuals. CONCLUSIONS The integration of ecological interactions derived from statistical models, extirpation dates from nonparametric tests, and the exhaustive analysis of historical information can be applied to define the current situation of imperiled, ecologically relevant species, in different aquatic ecosystems. We are confident that this general framework is important for determining (1) the requirements and limitations of populations regarding abiotic variables, (2) biotic interactions (trophic and spatial) with native and introduced species, and (3) different anthropogenic stressors within and around the ecosystem. This knowledge will also allow understanding those aspects that contribute to the extirpation of populations and could help the restoration of the habitat and the reintroduction of extirpated species.
时空格局和相互作用分析对于确定限制种群数量的非生物因素以及其他物种和不同人为压力源对物种灭绝的影响具有重要意义。对Hubbsina turneri de Buen鱼(1940)在不同地点的历史背景下作为模式物种进行了研究。本种原仅分布于墨西哥主要湖泊群Lerma-Chapala盆地，未在Cuitzeo湖(LC)采集，现仅分布于Zacapu湖(LZ)。目前，高原裂鳍被列为极度濒危物种。方法利用聚类分析和广义加性混合模型(GAMM)分别分析了llc的历史信息和LZ的历史和当前信息，分别描述了鱼类之间的生物相互作用以及密度与环境变量的关系。两湖不同的非生物/生物特征为描述化学离子梯度中某些物种的分布界限提供了元素。采用最优线性估计方法估计消光日历日期。最后，通过文献综述，分析了促使该物种灭绝和限制的原因，并对其重建和保护前景进行了展望。结果鱼群群根据其沿湖分布表现出相互关系。GAMM分析表明，高turneri密度与低硬度/粪便大肠菌群、中等深度/悬浮物和高氧浓度有关。估计灭绝日期在2013年至2018年之间。这种灭绝与LC体积的突然下降、水质退化、大型植物栖息地与本地和引进物种的生物相互作用增加以及渔业副渔获物有关。目前的限制范围是由于较大湖泊的排水，迫使剩余的种群以较小的泉水为生。最近在LZ的采样结果显示个体数量很少。结论综合统计模型得出的生态相互作用、非参数检验得出的灭绝日期以及对历史信息的详尽分析，可以确定不同水生生态系统中濒危、生态相关物种的现状。我们相信，这一总体框架对于确定(1)种群对非生物变量的需求和限制，(2)与本地和引进物种的生物相互作用(营养和空间)，以及(3)生态系统内部和周围不同的人为压力源很重要。这方面的知识还将有助于了解导致种群灭绝的那些方面，并有助于恢复生境和重新引进已灭绝的物种。
{"title":"Historical analysis of an imperiled fish species: environmental variables modeling, biotic interactions, extirpation, and current restricted-range.","authors":"R. Moncayo-Estrada, J. Cruz-Agüero, E. López-López, P. Monte-Luna, María Magdalena Díaz-Argüero, Arturo Chacón-Torres, A. Ramírez-García, O. Domínguez‐Domínguez, J. P. Ramírez-Herrejón","doi":"10.31083/j.fbl2705165","DOIUrl":"https://doi.org/10.31083/j.fbl2705165","url":null,"abstract":"BACKGROUND\u0000Analyses of spatial and temporal patterns and interactions are important for determining the abiotic factors limiting populations and the impact from other species and different anthropogenic stressors that promote the extirpation of species. The fish Hubbsina turneri de Buen (1940) was studied as a model species in a historical context at varying locations. Originally distributed only in the Lerma-Chapala basin, the main lake complex in Mexico, this species has not been collected from Lake Cuitzeo (LC) and now is restricted to Lake Zacapu (LZ). At present, the Highland splitfin is classified as critically endangered.\u0000\u0000\u0000METHODS\u0000Historical information of LC and historical and current information from LZ were explored by applying cluster analysis and generalized additive mixed model (GAMM) to describe the biotic interactions among fish species and the relationship between density and environmental variables, respectively. The two lakes' contrasting abiotic/biotic characteristics provided elements to describe some species distribution limits in chemical ion gradients. Extirpation calendar dates were estimated using an optimal linear estimation method. Finally, a bibliographic review was conducted on the causes that promoted the extirpation and restriction of H. turneri and the prognosis for its reestablishment and conservation.\u0000\u0000\u0000RESULTS\u0000Clusters showed the fishes relationship according to their distribution along the lakes. GAMM indicated that high H. turneri density is related to low hardness/fecal coliforms, medium depth/suspended solids, and high oxygen concentration. Estimated extirpation dates were between the years 2013 and 2018. The extirpation was linked to an abrupt drop in the LC volume, water quality degradation, increased biotic interactions within macrophytes habitats with native and introduced species, and fisheries bycatches. The current restricted range of H. turneri resulted from the draining of the larger lake, forcing the remaining populations to small spring-fed remnants. Recent samplings in LZ resulted in a low number of individuals.\u0000\u0000\u0000CONCLUSIONS\u0000The integration of ecological interactions derived from statistical models, extirpation dates from nonparametric tests, and the exhaustive analysis of historical information can be applied to define the current situation of imperiled, ecologically relevant species, in different aquatic ecosystems. We are confident that this general framework is important for determining (1) the requirements and limitations of populations regarding abiotic variables, (2) biotic interactions (trophic and spatial) with native and introduced species, and (3) different anthropogenic stressors within and around the ecosystem. This knowledge will also allow understanding those aspects that contribute to the extirpation of populations and could help the restoration of the habitat and the reintroduction of extirpated species.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"17 1","pages":"165"},"PeriodicalIF":3.1,"publicationDate":"2022-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80311766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Discs large MAGUK scaffold protein 5 (DLG5) is a multi-domain member of membrane-associated guanylate kinase (MAGUK) family, which plays a major role in the maintenance of cell epithelial polarity being part of the SCRIB-LGL-DLG complex. Although polarity proteins have been generally considered tumor suppressors, recent discoveries led to reconsidering their role in cancer. This is also true for DLG5 in different cancer types, including hepatocellular carcinoma (HCC). In this cancer, DLG5 was negatively associated with malignant characteristics, however recent findings associated DLG5 expression with advanced stages of HCC. In vitro studies evidenced its possible role in sustaining cell growth and migration by the interaction with several intracellular pathways, such as Hippo, Hedgehog, and PI3K/AKT signaling pathways. In this review, we summarize the recent finding on the dual role of DLG5 and other polarity proteins in cancers. What emerges is a still undefined role of those proteins in cancers, especially in HCC, one of the most frequent cancers worldwide, where the function of DLG5 and other polarity proteins is still largely unexplored.
{"title":"Recent Hints on the Dual Role of Discs Large MAGUK Scaffold Protein 5 in Cancers and in Hepatocellular Carcinoma.","authors":"Chiara Andolfi, C. Tiribelli, D. Pascut","doi":"10.31083/j.fbl2705164","DOIUrl":"https://doi.org/10.31083/j.fbl2705164","url":null,"abstract":"Discs large MAGUK scaffold protein 5 (DLG5) is a multi-domain member of membrane-associated guanylate kinase (MAGUK) family, which plays a major role in the maintenance of cell epithelial polarity being part of the SCRIB-LGL-DLG complex. Although polarity proteins have been generally considered tumor suppressors, recent discoveries led to reconsidering their role in cancer. This is also true for DLG5 in different cancer types, including hepatocellular carcinoma (HCC). In this cancer, DLG5 was negatively associated with malignant characteristics, however recent findings associated DLG5 expression with advanced stages of HCC. In vitro studies evidenced its possible role in sustaining cell growth and migration by the interaction with several intracellular pathways, such as Hippo, Hedgehog, and PI3K/AKT signaling pathways. In this review, we summarize the recent finding on the dual role of DLG5 and other polarity proteins in cancers. What emerges is a still undefined role of those proteins in cancers, especially in HCC, one of the most frequent cancers worldwide, where the function of DLG5 and other polarity proteins is still largely unexplored.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"114 1","pages":"164"},"PeriodicalIF":3.1,"publicationDate":"2022-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72909450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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