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Publication : C-type lectin-like receptor (CLEC)-2, the ligand of podoplanin, induces morphological changes in podocytes.

First Author  Tanaka K Year  2022
Journal  Sci Rep Volume  12
Issue  1 Pages  22356
PubMed ID  36572741 Mgi Jnum  J:351336
Mgi Id  MGI:7413662 Doi  10.1038/s41598-022-26456-9
Citation  Tanaka K, et al. (2022) C-type lectin-like receptor (CLEC)-2, the ligand of podoplanin, induces morphological changes in podocytes. Sci Rep 12(1):22356
abstractText  Podoplanin (PDPN) is intensely expressed on the podocyte membrane in an evolutionally conserved manner. CLEC-2, the endogenous ligand of PDPN, is highly expressed in platelets and also exists in a soluble form in plasma. Normally, podocytes are sequestered from CLEC-2, but when the glomerular barrier is injured, podocytes gain access to CLEC-2. We tested the effects of CLEC-2 in podocytes in vitro and in vivo. Cultured podocytes treated with Fc-CLEC-2 demonstrated that CLEC-2 induced the dephosphorylation of ezrin, radixin, and moesin (ERM) proteins. Podocytes treated with Fc-CLEC-2 also showed the dissociation of F-actin filaments from PDPN, F-actin degradation, detachment, and round morphology. Next, we perfused normal mouse kidney in vivo with FLAG-CLEC-2. CLEC-2 induced dephosphorylation of ERM and widening of the foot processes of podocytes. Platelets were detected by immunostaining for CD41 in the urine of mice with podocyte injury, indicating that podocytes can encounter platelets when glomeruli are injured. Collectively, these observations suggest that when platelets leak through the injured glomeruli, CLEC-2 from the platelets acts on PDPN in podocytes and induces morphological change and detachment, which may further aggravate podocyte injury. Thus, PDPN on podocytes may work as a leaked-platelet sensor.
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