Membranes smooth muscle, markers

Fung and colleagues examined the metabolic conversion of organic nitrates in sub-cellular fractions of bovine coronary artery smooth muscle cells [66, 67]. They found NO-generating capacity to be present in membrane fractions and, with the use of marker enzymes, identified plasma membrane as the primary location. The enzyme involved in bioconversion was not glutathione-S-transferase [68] and differed from those that catalyse activation of organic nitrites [69]. Partial purification [70] established that the molecular sizes of the native enzyme and subunits were approximately 200 kDa and 58 kDa respectively, and that enzymic activity depends on the presence of a free thiol group. 

All the major cell types (epithelial, endothelial, smooth muscle cells, pneumocytes, chondrocytes, fibroblasts) capable of producing connective tissues (e.g. cartilage, basement membrane, parenchymal stroma) are susceptible to oxidative injury in vitro [29- 33], and over the past decade the mechanism(s) of oxidative stress to these cell types has been the focus of intense research. Unfortunately, few of these studies have been specifically extended to examine the biochemical evidence for oxidative injury to connective tissue producing cells in vivo [34], Our most recent work has concentrated on determining the precise biochemical footprints of oxidative injury found within chondrocytes (also colonic epithelial cells) and attempting to correlate the presence or absence of these oxidative-injury markers seen in vitro with inflamed material from animal models and human pathological material. 

Evidence for the link between PKC activation and cell proliferation was initially provided by the demonstration that two intracellular events associated with cell replication - a rise in cytosolic pH and the expression of the proto-oncogenes c-fi/s and c-tnyc - are controlled by PKC PKC stimulates the membrane bound Na /H exchange mechanism in smooth muscle which extrudes intracellular H in exchange for extracellular Na this leads to a rise in intracellular pH, a prerequisite for cellular DNA replication (Mitsuka and Berk, 1991). c-fbs and c-myc are proto-oncogenes whose transcription to mRNA is one of the earliest markers of cell proliferation they encode for proteins, found in the cell nucleus, which initiate the sequence of events leading to DNA synthesis (Rozen-gurt, 1991). 

Perineurioma of the GI tract is a relatively recently described entity that rarely presents as a polypoid lesion. These lesions are composed of a bland spindle cell proliferation with delicate cytoplasmic protrusions that emanate from either side of an elongated nucleus. Like neurofibroma, this lesion grows around and entraps adjacent intestinal crypts. Analogous to perineuriomas of the soft tissues, intestinal perineuriomas almost uniformly stain with epithelial membrane antigen (EMA) a subset of these lesions expresses claudin-1. These lesions are negative for smooth muscle markers, S-100 protein, and c-kit. 

The involvement of pericytes in physiological or tumour angiogenesis is a matter of debate. Papoutsi et al. (2000) studied the expression of pericyte, smooth muscle cell and matrix markers in experimental tumours of the mammary ductal adenoma MDA-MB231 cell line grown on chick or quail chorioallantoic membrane. Pericyte-like cells may be attracted by MDA-MB231 cells during tumour angiogenesis but failed to interact properly with endothelial cells in the tumour environment (Lauer et al. 2000). 

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