Masudul Haque

Bio: Masudul Haque is an academic researcher from Louisiana State University. The author has contributed to research in topics: Oxidative stress & Angiotensin II. The author has an hindex of 15, co-authored 25 publications receiving 1122 citations.

Involvement of Tumor Necrosis Factor-α in Angiotensin II–Mediated Effects on Salt Appetite, Hypertension, and Cardiac Hypertrophy

Abstract: Hypertension is considered a low-grade inflammatory condition induced by various proinflammatory cytokines, including tumor necrosis factor (TNF)-alpha. Recent studies have implicated an involvement of TNF-alpha in the development of salt-sensitive hypertension induced by angiotensin II (Ang II). To understand further the relationship between TNF-alpha and Ang II, we examined the responses to Ang II in TNF-alpha knockout (TNF-alpha(-/-)) mice in the present study. A continuous infusion of Ang II (1 microg/kg per minute) for 2 weeks was given to both TNF-alpha(-/-) and wild-type (WT) mice with implanted osmotic minipumps. Daily measurement of water intake, salt intake, and urine output were performed using metabolic cages. Blood pressure was monitored continuously with implanted radiotelemetry. Ang II administration for 2 weeks caused increases in salt (0.2+/-0.07 to 5.6+/-0.95 mL/d) and water (5.4+/-0.34 to 11.5+/-1.2 mL/d) intake and in mean arterial pressure (115+/-1 to 151+/-3 mm Hg) in wild-type mice, but these responses were absent in TNF-alpha(-/-) mice (0.2+/-0.04 to 0.3+/-0.09 mL/d, 5.5+/-0.2 to 6.1+/-0.07 mL/d, and 113+/-2 to 123+/-3 mm Hg, respectively). Cardiac hypertrophy induced by Ang II was significantly attenuated in TNF-alpha(-/-) mice compared with wild-type mice. In a group of TNF-alpha(-/-) mice, when replacement therapy was made with recombinant TNF-alpha, Ang II induced similar responses in salt appetite, mean arterial pressure, and cardiac hypertrophy, as observed in wild-type mice. These results suggest that TNF-alpha plays a mechanistic role in mediating chronic Ang II-induced effects on salt appetite and blood pressure, as well as on cardiac hypertrophy.

TNF-α-induced mitochondrial oxidative stress and cardiac dysfunction : restoration by superoxide dismutase mimetic Tempol

Abstract: Mitochondria are indispensable for bioenergetics and for the regulation of physiological/signaling events in cellular life. Although TNF-α-induced oxidative stress and mitochondrial dysfunction are...

Chronic NF-κB blockade reduces cytosolic and mitochondrial oxidative stress and attenuates renal injury and hypertension in SHR

Abstract: Nuclear factor-κB (NF-κB) plays an important role in hypertensive renal injury; however, its roles in perpetuating mitochondrial oxidative stress and renal dysfunction remain unclear. In this study...

TNF-α blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats

Abstract: Oxidative stress plays an important role in the pathophysiology of cardiovascular disease. Recent evidence suggests that cytokines induce oxidative stress and contribute to cardiac dysfunction. In ...

Role of Proinflammatory Cytokines and Redox Homeostasis in Exercise-Induced Delayed Progression of Hypertension in Spontaneously Hypertensive Rats

Abstract: Hypertension is a well-known risk factor for various cardiovascular diseases. Recently, exercise has been recommended as a part of lifestyle modification for all hypertensive patients. However, the precise mechanisms of exercise training (ExT)-induced effects on the development of hypertension are poorly understood. Therefore, we hypothesized that chronic ExT would delay the progression of hypertension in young spontaneously hypertensive rats (SHRs). In addition, we explored whether the beneficial effects of chronic ExT were mediated by reduced proinflammatory cytokines and improved redox status. We also investigated the involvement of nuclear factor-kappaB in exercise-induced effects. To test our hypotheses, young normotensive (Wistar-Kyoto) and SHRs were given moderate-intensity ExT for 16 weeks. Blood pressure was determined by the tail-cuff method, and cardiac function was assessed by echocardiography. Myocardial total reactive oxygen species and superoxide production were measured by electron paramagnetic resonance spectroscopy; tumor necrosis factor-alpha, interleukin-1beta, gp91(phox), and inducible NO synthase by real-time PCR; and nuclear factor kappaB activity by electrophoretic mobility shift assay. Chronic ExT in hypertensive rats resulted in significantly reduced blood pressure, reduced concentric hypertrophy, and improved diastolic function. ExT significantly reduced proinflammatory cytokines and inducible NO synthase, attenuated total reactive oxygen species and superoxide production, and increased antioxidants in SHRs. ExT also resulted in increased NO production and decreased nuclear factor kappaB activity in SHRs. In summary, chronic ExT delays the progression of hypertension and improves cardiac function in young SHRs; these ExT-induced beneficial effects are mediated by reduced proinflammatory cytokines and improved redox homeostasis via downregulation of nuclear factor-kappaB.

The Central Nervous System

Abstract: Evolution of Nervous Control from Primitive Organisms to Man A Symposium organized by the Section on Medical Sciences of the American Association for the Advancement of Science, and presented at the New York Meeting on December 29–30, 1956. Edited by Allan D. Bass. Pp. vii + 231. (Washington, D.C.: American Association for the Advancement of Science; London: Bailey Bros. and Swinfen, Ltd., 1959.) 52s.

Molecular mechanism mediating proliferation, defferentiation interralationships during progressie development of the osteoblast phenotype

Abstract: I. Introduction A FUNCTIONAL relationship between cell growth and the initiation and progression of events associated with differentiation has been a fundamental question challenging developmental biologists for more than a century. In the case of bone, as observed with other cells and tissue, the relationship of growth and differentiation must be maintained and stringently regulated, both during development and throughout the life of the organism, to support tissue remodeling. For many years, bone was defined anatomically and examined largely in a descriptive manner by ultrastructural analysis and by biochemical and histochemical methods. These studies provided the basis for our understanding of bone tissue organization and orchestration of the progressive recruitment, proliferation, and differentiation of the various cellular components of bone tissue. Now, complemented by an increased knowledge of molecular mechanisms that are associated with and regulate expression of genes encoding phenotypic compone...

Interleukin 17 Promotes Angiotensin II–Induced Hypertension and Vascular Dysfunction

Abstract: We have shown previously that T cells are required for the full development of angiotensin II–induced hypertension. However, the specific subsets of T cells that are important in this process are unknown. T helper 17 cells represent a novel subset that produces the proinflammatory cytokine interleukin 17 (IL-17). We found that angiotensin II infusion increased IL-17 production from T cells and IL-17 protein in the aortic media. To determine the effect of IL-17 on blood pressure and vascular function, we studied IL-17−/− mice. The initial hypertensive response to angiotensin II infusion was similar in IL-17−/− and C57BL/6J mice. However, hypertension was not sustained in IL-17−/− mice, reaching levels 30-mm Hg lower than in wild-type mice by 4 weeks of angiotensin II infusion. Vessels from IL-17−/− mice displayed preserved vascular function, decreased superoxide production, and reduced T-cell infiltration in response to angiotensin II. Gene array analysis of cultured human aortic smooth muscle cells revealed that IL-17, in conjunction with tumor necrosis factor-α, modulated expression of >30 genes, including a number of inflammatory cytokines/chemokines. Examination of IL-17 in diabetic humans showed that serum levels of this cytokine were significantly increased in those with hypertension compared with normotensive subjects. We conclude that IL-17 is critical for the maintenance of angiotensin II–induced hypertension and vascular dysfunction and might be a therapeutic target for this widespread disease.

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.

Abstract: The renin-angiotensin-aldosterone system plays crucial roles in cardiovascular physiology and pathophysiology. However, many of the signaling mechanisms have been unclear. The angiotensin II (ANG I...