Browsing by Author "Harikrishnan, V. S."

Now showing 1 - 3 of 3
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    Adipogenesis on biphasic calcium phosphate using rat adipose-derived mesenchymal stem cells: In vitro and in vivo
    (JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A, 2012)
    Developing adipose tissue-engineered construct to mend soft tissue defects arising from traumatic injury, tumor resections, and maxillofacial abnormalities is of prime importance in plastic and reconstructive surgical procedures. It is apparent that the clinical outcome of classic techniques like adipose tissue transplantation is unpredictable, with graft resorption, lack of vascularization, and impaired functionality. In this prospective, the concept of tissue engineering was adopted to fabricate a combination product with biphasic calcium phosphate (BCP) and rat adipose-derived mesenchymal stem cells (ASCs) toward the development of an adipose tissue construct. BCP, a combination of hydroxyapatite and a-tricalcium phosphate, was characterized for its physiochemical properties, and ASCs were characterized for their stemness. The cellceramic interactions were demonstrated in vitro, whereas adipogenesis was picturesquely depicted by Nile red-stained multilocular adipocyte-like cells. Subsequently, the three-dimensional cellceramic-engineered construct was implanted in the rat dorsal muscle for a period of 3 weeks to demonstrate the efficacy of the tissue construct in vivo. Interestingly, the histology of the postimplanted tissue construct revealed the distribution of chicken wire net-like fat cells within the vicinity of the construct. The efficacy of cell transplantation via the scaffold was traced using fluorescent in situ hybridization by labeling the Y chromosome. Thus, the ceramic-based construct may be a good option for reconstruction therapies. (C) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A:, 2012.
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    Temporal relation of cardiac hypertrophy, oxidative stress, and fatty acid metabolism in spontaneously hypertensive rat
    (MOLECULAR AND CELLULAR BIOCHEMISTRY, 2011)
    Left ventricular hypertrophy is an adaptive response to hypertension, and an independent clinical risk factor for cardiac failure, sudden death, and myocardial infarction. As regression of cardiac hypertrophy is associated with a lower likelihood of cardiovascular events, it is recognized as a target of antihypertensive therapy. This necessitates identification of factors associated with the initiation and progression of hypertrophy. Oxidative stress and metabolic shift are intimately linked with myocardial hypertrophy, but their interrelationship is not clearly understood. This study proposes to identify the temporal sequence of events so as to distinguish whether oxidative stress and metabolic shift are a cause or consequence of hypertrophy. Spontaneously hypertensive rat (SHR) was used as the experimental model. Cardiac hypertrophy was apparent at 2 months of age, as assessed by hypertrophy index and brain natriuretic peptide gene expression. Enhanced myocardial lipid peroxidation accompanied by nuclear factor-kappa B gene expression in one-month-old SHR suggests that oxidative stress precedes the development of hypertrophy. Metabolic shift identified by reduction in the expression of peroxisome proliferator-activated receptor-alpha, medium chain acyl CoA dehydrogenase, and carnitine palmitoyltransferase 1 beta was seen at 4 months of age, implying that reduction of fatty acid oxidation is a consequence of hypertrophy. Information on the temporal sequence of events associated with hypertrophy will help in the prevention and reversal of cardiac remodeling. Investigations aimed at prevention of hypertrophy should address reduction of oxidative stress. Both, oxidative stress and metabolic modulation have to be considered for studies that focus on the regression of hypertrophy.