PubMed · 5826371
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P Meriel, G Moreau, J M Suc, J Putois, J Conte. [The intercapillary tissue].. https://pubmed.ncbi.nlm.nih.gov/5826371/
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In preeclampsia, invasion of intrauterine decidual blood vessels by placental cytotrophoblasts is significantly reduced. This study examined the secretion of matrix metalloproteinases (MMP) by cultured human decidual endothelial cells from normal (NDEC) and preeclamptic (PEDEC) pregnancies. MMPs secreted into the culture medium were measured using zymography, Western blotting, and ELISA. Results were confirmed by Northern analysis. Phorbol myristate acetate, known to induce protease activity in other endothelial cell populations, stimulated MMP1, MMP9, and TIMP1 secretion in both NDEC and PEDEC. Neither tumor necrosis factor-alpha nor transforming growth factor-beta, both thought to have significant roles in the control of placentation, affected MMP secretion. MMP9 and TIMP1 levels were similar between the two cell types; however, MMP1 secretion was markedly different between the cell types. NDEC expressed higher levels of MMP1 under both basal (160 +/- 32 ng/10(6) cells) and stimulated (275 +/- 50) conditions compared to PEDEC (32 +/- 24 and 70 +/- 53, respectively). The lower MMP1 expression of decidual endothelial cells from preeclamptic women may inhibit endovascular invasion by cytotrophoblasts. These findings may, at least partly, explain the relative failure of trophoblasts to invade maternal decidual blood vessels in preeclamptic pregnancy.
A 58 year old patient with hepatitis virus C (HCV) infection had a secondary polyclonal IgG-IgM cryoglobulinemia with a benign 20 year course. Clinically the patient suffered from progressive pigmented purpura (PPP). Histologic evaluation revealed a lymphocytic vasculitis. Food containing tartrazine triggered flares of the PPP, as demonstrated with controlled oral provocation testing. In most of the previously described cases of HCV and type III cryoglobulinemia, the typical cutaneous finding was palpable purpura with leukocytoclastic vasculitis.
Since we reported a case of acute relaxant-steroid myopathy (ARSM) in 1994, we continued histological studies and compared the findings with those in a case of corticosteroid myopathy (CM). It was revealed that (1) dystrophin, spectrin, beta dystroglycan, and sarcoglycans on the cell surface were decreased, (2) regular arrangement of the sarcoplasmic reticulum was lost, and (3) some capillaries were degenerated. Since none of these changes were seen in CM, it became clear that ARSM is different from CM. It was estimated that continuous administration of non-depolarizing muscle relaxant produces a state akin to denervation. Combination of denervation, immobilization and circulatory disturbance in ARSM not only augments the effects of corticosteroids, but they produce changes different from CM, namely impairment of the cell membrane system (both internal and external) and capillary degeneration.