Journal
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Volume 85, Issue 1, Pages -Publisher
WILEY
DOI: 10.1111/aji.13325
Keywords
calpain; calpastatin; fetal growth restriction; infarction; placenta
Categories
Funding
- JSPS KAKENHI [JP20591924]
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The study revealed that activation of mu-calpain is suppressed in FGR placentas, and calpain-6 in human placenta is involved in the pathology of FGR.
Problem: The mechanism of fetal growth restriction (FGR) is not fully understood. In this study, we explored the contribution of the calpain-calpastatin system and the activated states of calpains in human FGR placenta. Method of study: The placentas were collected from patients of FGR (n = 17) and controls (n = 23) at elective cesarean sections in Nagoya City University Hospital and used for experiments upon informed consent. The existence and the expression of calpains and calpastatin in human placenta were compared between FGR and controls using immunohistochemistry, SDS-PAGE, and Western blotting. Results: Staining of calpains (pre-, post-mu-calpain, pre-, post-m-calpain, and calpain-6) and calpastatin was observed in cytoplasm of trophoblast cells, both in FGR and control placenta. Pre-mu-calpain was located in the cytoplasm, and post-mu-calpain was located mainly in proximity to the cytoplasmic membrane. The expression of pre-mu-calpain was significantly higher (P < .001) and calpain-6 was significantly lower (P = .01) in FGR placentas. The inactive mu-calpain (80 kDa) was significantly elevated (P < .01), and active mu-calpain (76 kDa) was significantly decreased (P = .01) in FGR placentas. Conclusion: The results demonstrate that activation of mu-calpain is suppressed in FGR placentas and that calpain-6 in human placenta is involved in the pathology of FGR.
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