Pub Date : 2024-09-12DOI: 10.1152/ajprenal.00172.2024
Andrew Beenken, Tian Shen, Guangchun Jin, Aryan Ghotra, Katherine Xu, Kivanc Nesanir, Rachel E. Sturley, Soundarapandian Vijayakumar, Atlas Kahn, Abraham Levitman, Jacob Stauber, Estefania Y. Chavez, Shelief Y. Robbins-Juarez, Luke Hao, Thomas B. Field, Hediye Erdjument-Bromage, Thomas A. Neubert, Lawrence Shapiro, Andong Qiu, Jonathan Barasch
American Journal of Physiology-Renal Physiology, Ahead of Print.
美国生理学杂志-肾脏生理学》，提前出版。
{"title":"Spns1 is an iron transporter essential for megalin-dependent endocytosis.","authors":"Andrew Beenken, Tian Shen, Guangchun Jin, Aryan Ghotra, Katherine Xu, Kivanc Nesanir, Rachel E. Sturley, Soundarapandian Vijayakumar, Atlas Kahn, Abraham Levitman, Jacob Stauber, Estefania Y. Chavez, Shelief Y. Robbins-Juarez, Luke Hao, Thomas B. Field, Hediye Erdjument-Bromage, Thomas A. Neubert, Lawrence Shapiro, Andong Qiu, Jonathan Barasch","doi":"10.1152/ajprenal.00172.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00172.2024","url":null,"abstract":"American Journal of Physiology-Renal Physiology, Ahead of Print. <br/>","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215743","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}
Pub Date : 2024-09-12DOI: 10.1152/ajprenal.00088.2024
Anna Billeschou Bomholt, Christian Dall Johansen, Katrine Douglas Galsgaard, Emilie Elmelund, Marie Winther-Sørensen, Jens Juul Holst, Nicolai J. Wewer Albrechtsen, Charlotte Mehlin Sorensen
American Journal of Physiology-Renal Physiology, Ahead of Print.
美国生理学杂志-肾脏生理学》，提前出版。
{"title":"Glucagon receptor activation contributes to the development of kidney injury","authors":"Anna Billeschou Bomholt, Christian Dall Johansen, Katrine Douglas Galsgaard, Emilie Elmelund, Marie Winther-Sørensen, Jens Juul Holst, Nicolai J. Wewer Albrechtsen, Charlotte Mehlin Sorensen","doi":"10.1152/ajprenal.00088.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00088.2024","url":null,"abstract":"American Journal of Physiology-Renal Physiology, Ahead of Print. <br/>","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"35 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215744","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}
Pub Date : 2024-09-12DOI: 10.1152/ajprenal.00204.2024
Hannah A. Anderson, Gabriella L. Robilotto, Aaron D. Mickle
American Journal of Physiology-Renal Physiology, Ahead of Print.
美国生理学杂志-肾脏生理学》，提前出版。
{"title":"Role of Local Angiotensin II Signaling in Bladder Function","authors":"Hannah A. Anderson, Gabriella L. Robilotto, Aaron D. Mickle","doi":"10.1152/ajprenal.00204.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00204.2024","url":null,"abstract":"American Journal of Physiology-Renal Physiology, Ahead of Print. <br/>","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"279 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215717","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}
Pub Date : 2024-09-12DOI: 10.1152/ajprenal.00143.2024
Shaoqun Shu, Hui Wang, Juan Cai, Anqun Chen, Zheng Dong
American Journal of Physiology-Renal Physiology, Ahead of Print.
美国生理学杂志-肾脏生理学》，提前出版。
{"title":"Establishment and characterization of a mouse model for studying kidney repair in diabetes","authors":"Shaoqun Shu, Hui Wang, Juan Cai, Anqun Chen, Zheng Dong","doi":"10.1152/ajprenal.00143.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00143.2024","url":null,"abstract":"American Journal of Physiology-Renal Physiology, Ahead of Print. <br/>","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"161 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215745","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}
Pub Date : 2024-05-09DOI: 10.1152/ajprenal.00121.2024
Lashodya V. Dissanayake, Oleg Palygin
American Journal of Physiology-Renal Physiology, Ahead of Print.
美国生理学杂志-肾脏生理学》，提前出版。
{"title":"Is there a role for uric acid in polycystic kidney disease progression?","authors":"Lashodya V. Dissanayake, Oleg Palygin","doi":"10.1152/ajprenal.00121.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00121.2024","url":null,"abstract":"American Journal of Physiology-Renal Physiology, Ahead of Print. <br/>","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140925593","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}
Pub Date : 2024-05-02DOI: 10.1152/ajprenal.00383.2023
Zoé Oulerich, Amanda N. Sferruzzi-Perri
According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, exposure to certain environmental influences during early life may be a key determinant of fetal development and short- and long-term offspring health. Indeed, adverse conditions encountered during the fetal, perinatal, and early childhood stages can alter normal development and growth, as well as put the offspring at elevated risk of developing long-term health conditions in adulthood, including chronic kidney disease (CKD) and cardiovascular diseases. Of relevance in understanding the mechanistic basis of these long-term health conditions, are previous findings showing low glomerular number in human intrauterine growth restriction and low birth weight - indicators of a sub-optimal intrauterine environment. In different animal models, the main sub-optimal intrauterine conditions studied relate to maternal dietary manipulations, poor micronutrient intake, prenatal ethanol exposure, maternal diabetes, glucocorticoid and chemical exposure, hypoxia, and placental insufficiency. These studies have demonstrated changes in kidney structure, glomerular endowment, and expression of key genes and signalling pathways controlling endocrine, excretion and filtration function of the offspring. This review aims to summarize those studies to uncover the effects and mechanisms by which adverse gestational environments impact offspring renal and vascular health in adulthood. This is important for identifying agents and interventions that can prevent and mitigate the long-term consequences of an adverse intrauterine environment on the subsequent generation.
{"title":"Early-life exposures and long-term health: adverse gestational environments and the programming of offspring renal and vascular disease","authors":"Zoé Oulerich, Amanda N. Sferruzzi-Perri","doi":"10.1152/ajprenal.00383.2023","DOIUrl":"https://doi.org/10.1152/ajprenal.00383.2023","url":null,"abstract":"According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, exposure to certain environmental influences during early life may be a key determinant of fetal development and short- and long-term offspring health. Indeed, adverse conditions encountered during the fetal, perinatal, and early childhood stages can alter normal development and growth, as well as put the offspring at elevated risk of developing long-term health conditions in adulthood, including chronic kidney disease (CKD) and cardiovascular diseases. Of relevance in understanding the mechanistic basis of these long-term health conditions, are previous findings showing low glomerular number in human intrauterine growth restriction and low birth weight - indicators of a sub-optimal intrauterine environment. In different animal models, the main sub-optimal intrauterine conditions studied relate to maternal dietary manipulations, poor micronutrient intake, prenatal ethanol exposure, maternal diabetes, glucocorticoid and chemical exposure, hypoxia, and placental insufficiency. These studies have demonstrated changes in kidney structure, glomerular endowment, and expression of key genes and signalling pathways controlling endocrine, excretion and filtration function of the offspring. This review aims to summarize those studies to uncover the effects and mechanisms by which adverse gestational environments impact offspring renal and vascular health in adulthood. This is important for identifying agents and interventions that can prevent and mitigate the long-term consequences of an adverse intrauterine environment on the subsequent generation.","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"60 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140829482","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}
Pub Date : 2024-05-02DOI: 10.1152/ajprenal.00057.2024
Yvonne Zuchowski, Joshua Carty, Jonathan B. Trapani, Jason Watts, Fabian Bock, Mingzhi Zhang, Andrew Terker, Roy Zent, Eric Delpire, Raymond C. Harris, Juan Pablo Arroyo
We previously showed that kidney collecting ducts make vasopressin. However, the physiologic role of collecting-duct-derived vasopressin is uncertain. We hypothesized that collecting-duct-derived vasopressin was required for appropriate concentration of urine. We developed a vasopressin conditional knockout mouse model wherein Cre recombinase expression induces deletion of Avp exon 1 in the distal nephron. We then used age-matched 8 - 12 week old Avp fl/fl;Ksp-Cre(-) (WT) and Avp fl/fl;Ksp-Cre(+) mice for all experiments. We collected urine, serum, and kidney lysates at baseline. We then challenged both WT and KO mice with 24 hour water restriction, water loading, and administration of the vasopressin type 2 receptor (V2R) agonist desmopressin (dDAVP) 1 µg/kg/ip) followed by V2R antagonist OPC-31260 (10 mg/kg/ip). We performed immunofluorescence and immunoblot analysis at baseline and confirmed vasopressin knockout in the collecting duct. We found that urinary osmolality (UOsm), plasma Na+, K+, Cl-, BUN, and copeptin were similar in WT vs KO mice at baseline. Immunoblots of vasopressin regulated proteins Na:K:2Cl cotransporter (NKCC2), Na:Cl cotransporter (NCC) and water channel aquaporin-2 (AQP2) showed no difference in expression or phosphorylation at baseline. Following 24 hour water restriction, WT and KO mice had no differences in UOsm, plasma Na+, K+, Cl-, BUN or copeptin. Additionally, there were no differences in the rate of urinary concentration or dilution as WT and KO mice UOsm was nearly identical after dDAVP and OPC-31260 administration. We conclude that collecting-duct-derived vasopressin is not essential to appropriately concentrate or dilute urine.
{"title":"Kidney collecting-duct-derived vasopressin is not essential for appropriate concentration or dilution of urine","authors":"Yvonne Zuchowski, Joshua Carty, Jonathan B. Trapani, Jason Watts, Fabian Bock, Mingzhi Zhang, Andrew Terker, Roy Zent, Eric Delpire, Raymond C. Harris, Juan Pablo Arroyo","doi":"10.1152/ajprenal.00057.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00057.2024","url":null,"abstract":"We previously showed that kidney collecting ducts make vasopressin. However, the physiologic role of collecting-duct-derived vasopressin is uncertain. We hypothesized that collecting-duct-derived vasopressin was required for appropriate concentration of urine. We developed a vasopressin conditional knockout mouse model wherein Cre recombinase expression induces deletion of <i>Avp</i> exon 1 in the distal nephron. We then used age-matched 8 - 12 week old <i>Avp</i> fl/fl;<i>Ksp</i>-Cre(-) (WT) and <i>Avp</i> fl/fl;<i>Ksp</i>-Cre(+) mice for all experiments. We collected urine, serum, and kidney lysates at baseline. We then challenged both WT and KO mice with 24 hour water restriction, water loading, and administration of the vasopressin type 2 receptor (V2R) agonist desmopressin (dDAVP) 1 µg/kg/ip) followed by V2R antagonist OPC-31260 (10 mg/kg/ip). We performed immunofluorescence and immunoblot analysis at baseline and confirmed vasopressin knockout in the collecting duct. We found that urinary osmolality (UOsm), plasma Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>-</sup>, BUN, and copeptin were similar in WT vs KO mice at baseline. Immunoblots of vasopressin regulated proteins Na:K:2Cl cotransporter (NKCC2), Na:Cl cotransporter (NCC) and water channel aquaporin-2 (AQP2) showed no difference in expression or phosphorylation at baseline. Following 24 hour water restriction, WT and KO mice had no differences in UOsm, plasma Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>-</sup>, BUN or copeptin. Additionally, there were no differences in the rate of urinary concentration or dilution as WT and KO mice UOsm was nearly identical after dDAVP and OPC-31260 administration. We conclude that collecting-duct-derived vasopressin is not essential to appropriately concentrate or dilute urine.","PeriodicalId":7583,"journal":{"name":"American Journal of Physiology - Renal Physiology","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140829633","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：