Indeed, reductions in cardiovascular LB-100 molecular weight risk and rates of onset of new cases of diabetes mellitus have been reported in trials in patients with hypertension treated with CCAs. These beneficial effects extend beyond those expected to accompany reductions in BP.
Until recently, the biochemical effects underlying these metabolic changes were only poorly understood, but pharmacologic studies have now started to shed more light on these issues.
Of particular interest are studies with manidipine, some of which suggest that this agent may be associated with greater improvements in insulin sensitivity and may have better renal protective properties than other CCAs. Confirmation of potential differences among selective HDAC inhibitors CCAs in terms of the relative magnitude of any beneficial metabolic effects requires further study.
Ongoing research is expected to clarify further the action of these agents at the cellular level and to assist with the optimization of antihypertensive therapy, particularly in patients with elevated cardiovascular risk profiles.”
“Study Design.
To demonstrate the existence of mesenchymal stem cells (MSCs) in ligamentum flavum (LF) and their pathogenic role in LF hypertrophy.
Objective. To isolate and characterize LF-derived MSCs and their response to transforming growth factor-beta 1 (TGF-beta 1) and trichostatin A (TSA), a histone deacetylase inhibitor (HDACi).
Summary of Background Data. LF is a connective tissue, of which hypertrophic changes induce spinal stenosis. The pathogenic role of TGF-beta 1 in spinal stenosis has been implicated. TSA has been shown to suppress TGF-beta 1-induced alpha-smooth muscle actin (alpha-SMA), type I and III collagen synthesis in a variety of cells. MSCs have been isolated from a variety of adult tissues, except LF. Whether MSCs exist in LF and their response to TGF-beta 1 and TSA is not clear.
Methods. The MSCs
from LF were isolated and cultured. Their phenotypic character, linage differentiation potential, and response to TGF-beta 1 and TSA were analyzed.
Results. LF-derived MSCs have the similar profile of surface markers as bone marrow MSCs. They were demonstrated to have the potential to be differentiated into osteoblasts, adipocytes, and chondrocytes. Administration of TGF-beta 1 stimulated HIF inhibitor cell proliferation, enhanced the gene expression of type I and III collagen, and increased the gene expression and protein level of a-SMA. TSA blocked the fibrogenic effects of TGF-beta 1.
Conclusion. The current results demonstrated the isolation of MSCs from LF. The cellular response to TGF-beta 1 implied that these cells might play an important role in the pathogenesis of LF hypertrophy. TSA, which blocks the effects of TGF-beta 1, may be a potent therapeutic choice for inhibiting LF hypertrophy.”
“Background: Epidemiologic evidence suggests that prenatal growth influences adult blood pressure.