Semaphorin-3C Is Upregulated in Polycystic Kidney Epithelial Cells and Inhibits Angiogenesis of Glomerular Endothelial Cells
- Authors
- Kim, Bo Hye; Kim, Do Yeon; Ahn, Yejin; Lee, Eun Ji; Park, Hyunjoo; Park, Meeyoung; Park, Jong Hoon
- Issue Date
- Jul-2020
- Publisher
- KARGER
- Keywords
- Semaphorin-3c; Polycystic kidney disease; Proliferation; Angiogenesis
- Citation
- AMERICAN JOURNAL OF NEPHROLOGY, v.51, no.7, pp 556 - 564
- Pages
- 9
- Journal Title
- AMERICAN JOURNAL OF NEPHROLOGY
- Volume
- 51
- Number
- 7
- Start Page
- 556
- End Page
- 564
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/1363
- DOI
- 10.1159/000508263
- ISSN
- 0250-8095
1421-9670
- Abstract
- Background:Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner.Methods:To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD epithelial cells were used for further analysis, and GECs were exposed to recombinant SEMA3C (rSEMA3C). Also, co-culture and treatment of conditioned media were employed to confirm whether PKD epithelial cells could influence on GECs via SEMA3C secretion.Results:SEMA3C knockdown reduced proliferation of PKD epithelial cells. In case of GECs, exposure to rSEMA3C decreased angiogenesis, which resulted from suppressed migratory ability not cell proliferation.Conclusions:This study indicates that SEMA3C is the aggravating factor in PKD. Thus, it is proposed that targeting SEMA3C can be effective to mitigate PKD.
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