Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation
Preterm birth was previously identified as a high-risk factor for the long-term development of chronic kidney disease. However, the detailed pattern of podocyte (PD) changes caused by preterm birth and the potential mechanism underlying this process have not been well clarified. In present study, a...
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Frontiers Media S.A.
2023-03-01
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Series: | Frontiers in Cell and Developmental Biology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2023.1142929/full |
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author | Lulu Zhang Lulu Zhang Lulu Zhang Zhihui Chen Zhihui Chen Zhihui Chen Qi Gao Qi Gao Qi Gao Ge Liu Ge Liu Ge Liu Jun Zheng Jun Zheng Jun Zheng Fangrui Ding Fangrui Ding Fangrui Ding |
author_facet | Lulu Zhang Lulu Zhang Lulu Zhang Zhihui Chen Zhihui Chen Zhihui Chen Qi Gao Qi Gao Qi Gao Ge Liu Ge Liu Ge Liu Jun Zheng Jun Zheng Jun Zheng Fangrui Ding Fangrui Ding Fangrui Ding |
author_sort | Lulu Zhang |
collection | DOAJ |
description | Preterm birth was previously identified as a high-risk factor for the long-term development of chronic kidney disease. However, the detailed pattern of podocyte (PD) changes caused by preterm birth and the potential mechanism underlying this process have not been well clarified. In present study, a rat model of preterm birth was established by delivery of pups 2 days early and podometric methods were applied to identify the changes in PDs number caused by preterm birth. In addition, single-cell RNA sequencing (scRNA-seq) and subsequent bioinformatic analysis were performed in the preterm rat kidney to explore the possible mechanism caused by preterm birth. As results, when the kidney completely finished nephrogenesis at the age of 3 weeks, a reduction in the total number of differentiated PDs in kidney sections was detected. In addition, 20 distinct clusters and 12 different cell types were identified after scRNA-seq in preterm rats (postnatal day 2) and full-term rats (postnatal day 0). The numbers of PDs and most types of inherent kidney cells were decreased in the preterm birth model. In addition, 177 genes were upregulated while 82 genes were downregulated in the PDs of full-term rats compared with those of preterm rats. Further functional GO analysis revealed that ribosome-related genes were enriched in PDs from full-term rats, and kidney development-related genes were enriched in PDs from preterm rats. Moreover, known PD-specific and PD precursor genes were highly expressed in PDs from preterm rats, and pseudotemporal analysis showed that PDs were present earlier in preterm rats than in full-term rats. In conclusion, the present study showed that preterm birth could cause a reduction in the number of differentiated PDs and accelerate the differentiation of PDs. |
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spelling | doaj.art-90f09eb1a9fe40a297552db0354a8cc72023-03-02T07:03:04ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2023-03-011110.3389/fcell.2023.11429291142929Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiationLulu Zhang0Lulu Zhang1Lulu Zhang2Zhihui Chen3Zhihui Chen4Zhihui Chen5Qi Gao6Qi Gao7Qi Gao8Ge Liu9Ge Liu10Ge Liu11Jun Zheng12Jun Zheng13Jun Zheng14Fangrui Ding15Fangrui Ding16Fangrui Ding17Department of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaDepartment of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaDepartment of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaDepartment of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaDepartment of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaDepartment of Neonatology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, ChinaTianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, ChinaDepartment of Neonatology, Nankai University Maternity Hospital, Tianjin, ChinaPreterm birth was previously identified as a high-risk factor for the long-term development of chronic kidney disease. However, the detailed pattern of podocyte (PD) changes caused by preterm birth and the potential mechanism underlying this process have not been well clarified. In present study, a rat model of preterm birth was established by delivery of pups 2 days early and podometric methods were applied to identify the changes in PDs number caused by preterm birth. In addition, single-cell RNA sequencing (scRNA-seq) and subsequent bioinformatic analysis were performed in the preterm rat kidney to explore the possible mechanism caused by preterm birth. As results, when the kidney completely finished nephrogenesis at the age of 3 weeks, a reduction in the total number of differentiated PDs in kidney sections was detected. In addition, 20 distinct clusters and 12 different cell types were identified after scRNA-seq in preterm rats (postnatal day 2) and full-term rats (postnatal day 0). The numbers of PDs and most types of inherent kidney cells were decreased in the preterm birth model. In addition, 177 genes were upregulated while 82 genes were downregulated in the PDs of full-term rats compared with those of preterm rats. Further functional GO analysis revealed that ribosome-related genes were enriched in PDs from full-term rats, and kidney development-related genes were enriched in PDs from preterm rats. Moreover, known PD-specific and PD precursor genes were highly expressed in PDs from preterm rats, and pseudotemporal analysis showed that PDs were present earlier in preterm rats than in full-term rats. In conclusion, the present study showed that preterm birth could cause a reduction in the number of differentiated PDs and accelerate the differentiation of PDs.https://www.frontiersin.org/articles/10.3389/fcell.2023.1142929/fullpretermpodocytechronic kidney diseasesingle cell sequence (scRNA-seq)ribosome |
spellingShingle | Lulu Zhang Lulu Zhang Lulu Zhang Zhihui Chen Zhihui Chen Zhihui Chen Qi Gao Qi Gao Qi Gao Ge Liu Ge Liu Ge Liu Jun Zheng Jun Zheng Jun Zheng Fangrui Ding Fangrui Ding Fangrui Ding Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation Frontiers in Cell and Developmental Biology preterm podocyte chronic kidney disease single cell sequence (scRNA-seq) ribosome |
title | Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
title_full | Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
title_fullStr | Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
title_full_unstemmed | Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
title_short | Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
title_sort | preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation |
topic | preterm podocyte chronic kidney disease single cell sequence (scRNA-seq) ribosome |
url | https://www.frontiersin.org/articles/10.3389/fcell.2023.1142929/full |
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