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| 1 | Pulmonary hypertension and metabolic syndrome: Possible connection, PPARγ and Caveolin-1显示文摘A number of disparate diseases can lead to pulmonary hypertension(PH), a serious disorder with a high morbidity and mortality rate. Recent studies suggest that the associated metabolic dysregulation may be an important factor adversely impacting the prognosis of PH. Furthermore, metabolic syndrome is associated with vascular diseases including PH. Inflammation plays a significant role both in PH and metabolic syndrome. Adipose tissue modulates lipid and glucose metabolism, and also produces pro-and anti-inflammatory adipokines that modulate vascular function and angiogenesis, suggesting a close functional relationship between the adipose tissue and the vasculature. Both caveolin-1, a cell membrane scaffolding protein and peroxisome proliferator-activated receptor(PPAR) γ, a ligandactivated transcription factor are abundantly expressed in the endothelial cells and adipocytes. Both caveolin-1 and PPARγ modulate proliferative and anti-apoptotic pathways, cell migration, inflammation, vascular homeostasis, and participate in lipid transport, triacylglyceride synthesis and glucose metabolism. Caveolin-1 and PPARγ regulate the production of adipokines and in turn are modulated by them. This review article summarizes the roles and inter-relationships of caveolin-1,PPARγ and adipokines in PH and metabolic syndrome. | Rajamma Mathew | 2014 | World Journal of Cardiology2014，6，8： | 7 |
| 2 | Hematological disorders and pulmonary hypertension显示文摘Pulmonary hypertension(PH),a serious disorder with a high morbidity and mortality rate,is known to occur in a number of unrelated systemic diseases.Several hematological disorders such as sickle cell disease,thalassemia and myeloproliferative diseases develop PH which worsens the prognosis.Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction.Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity,activation of proliferative and antiapoptotic pathways leading to vascular remodeling,elevated pulmonary artery pressure,right ventricular hypertrophy and premature death.Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide(NO),limiting its bioavailability,and leading to endothelial dysfunction.In addition,hemolysis releases arginase into the circulation which converts L-arginine to ornithine,thus bypassing NO production.Furthermore,treatments for hematological disorders such as immunosuppressive therapy,splenectomy,bone marrow transplantation,and radiation have been shown to contribute to the development of PH.Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension(PAH).Several studies have reported low iron levels in patients with idiopathic PAH,and iron deficiency is an important risk factor.This article reviews PH associated with hematological disorders and its mechanism:and iron homeostasis and its relevance to PH. | Rajamma Mathew Jing Huang Joseph M Wu John T Fallon Michael H Gewitz | 2016 | World Journal of Cardiology2016，8，12： | 6 |
| 3 | Enhanced caveolin-1 expression in smooth muscle cells: Possible prelude to neointima formation显示文摘AIM: To study the genesis of neointima formation in pulmonary hypertension(PH), we investigated the role of caveolin-1 and related proteins. METHODS: Male Sprague Dawley rats were given monocrotaline(M, 40 mg/kg) or subjected to hypobaric hypoxia(H) to induce PH. Another group was given M and subjected to H to accelerate the disease process(M + H). Right ventricular systolic pressure, right ventricular hypertrophy, lung histology for medial hypertrophy and the presence of neointimal lesions were examined at 2 and 4 wk. The expression of caveolin-1 and its regulatory protein peroxisome proliferator-activated receptor(PPAR) γ, caveolin-2, proliferative and antiapoptotic factors(PY-STAT3, p-Erk, Bcl-x L), endothelial nitric oxide synthase(e NOS) and heat shock protein(HSP) 90 in the lungs were analyzed, and the results from M + H group were compared with the controls, M and H groups. Double immunofluorescence technique was used to identify the localization of caveolin-1 in pulmonary arteries in rat lungs and in human PH lung tissue. RESULTS: In the M + H group, PH was more severe compared with M or H group. In the 4 wk M+H group, several arteries with reduced caveolin-1 expression in endothelial layer coupled with an increased expression in smooth muscle cells(SMC), exhibited neointimal lesions. Neointima was present only in the arteries exhibiting enhanced caveolin-1 expression in SMC. Lung tissue obtained from patients with PH also revealed neointimal lesions only in the arteries exhibiting endothelial caveolin-1 loss accompanied by an increased caveolin-1 expression in SMC. Reduction in e NOS and HSP90 expression was present in the M groups(2 and 4 wk), but not in the M + H groups. In both M groups and in the M + H group at 2 wk, endothelial caveolin-1 loss was accompanied by an increase in PPARγ expression. In the M + H group at 4 wk, increase in caveolin-1 expression was accompanied by a reduction in the PPARγ expression. In the H group, there was neither a loss of endothelial caveolin-1, eNOS or HSP 90, nor an increase in SMC caveolin-1 expression; or any alteration in PPARγ expression. Proliferative pathways were activated in all experimental groups. CONCLUSION: Enhanced caveolin-1 expression in SMC follows extensive endothelial caveolin-1 loss with subsequent neointima formation. Increased caveolin-1 expression in SMC, thus, may be a prelude to neointima formation. | Jing Huang John H Wolk Michael H Gewitz James E Loyd James West Eric D Austin Rajamma Mathew | 2015 | World Journal of Cardiology2015，7，10： | 2 |
| 4 | Biology of spiraling whitefly,Aleurodicus disperses Russell (Homoptera:Aleyrodidae)显示文摘 | Rajamma P Rajasree K M Jayaprakas C A | 2002 | Journal of Root Crops2002，28，1： | 1 |
| 5 | Pulmonary artery hyperten- sion : caveolin-1 and eNOS interrelationship : a new perspec- tive 显示文摘 | Rajamma M Jing H Michael G | 2007 | Cardio in Review2007，15，3： | 1 |
| 6 | New technique in the control of sweet potato weevil using synthetic sex pheromone in India显示文摘 | Pillai K S Rajamma P Palaniswami M S | 1993 | International Journal of Pest Management1993，39，1： | 1 |
| 7 | Comparative larvicidal activity of different species of Ocimum against Culex Quinquefasciatus显示文摘 | A.J. Rajamma Sonal Dubey S.B. Sateesha S.N. Tiwari S.K. Ghosh | 2011 | Natural Product Research2011，，20： | 1 |
| 8 | Biology of spiraling whitefly, Aleurodicus disperses Russell (Homoptera: Aleyrodidae)显示文摘 | Rajamma P Rajasree K M Jayaprakas C A | 2002 | Journal of Root Crops2002，28，1： | 1 |
| 9 | Cell-Specific Dual Role of Caveolin-1 in Pulmonary Hypertension显示文摘 | Rajamma Mathew Andrew J. Halayko | 2011 | Pulmonary Medicine2011，，： | 1 |
| 10 | Progressive endothelial cell damage in an inflammatory model of pulmonary hypertension显示文摘 | Jing Huang John H. Wolk Michael H. Gewitz Rajamma Mathew | 2010 | Experimental Lung Research2010，，1： | 1 |
| 11 | Biology of spiralingwhitefly, Aleurodicus dispersus Russell (Homoptera: Aleyrodidae) 显示文摘 | Rajamma P Rajasree K M Jayaprakas C A | 2002 | Indian Society for Root Crops2002，28，1： | 1 |
| 12 | Biology ofspiraling whitefly, Aleurodicus dispersus Russell (Homoptera: Aleyrodidae)显示文摘 | Rajamma P Rajasree K M Jayaprakas C A | 2002 | Journal of Root Crops2002，28，1： | 1 |
| 13 | Biology of spiraling whitefly, Aleurodicus disperses Russell (Homoptera: Aleyrodidae)显示文摘 | Rajamma P Rajasree K M Jayaprakas C A | 2002 | Journal of Root Crops2002，28，1： | 1 |
| 14 | Enhanced visible light photocatalytic activity of Ga, N and S codoped TiOz for degradation of azo dye显示文摘 | Suresh S Umare Archana Charanpahari Rajamma Sasika- la | 2013 | Materi- als Chemistry and Physics2013，140，23： | 1 |
| 15 | Learned Ethical Behavior: An Academic Perspective 显示文摘 | Gundersun D E Capozzoli E A Rajamma R K | 2008 | Journal of Education for Business2008，83，6： | 1 |
| 16 | Cubic phase indium doped cadmium sulfide dispersed on zinc oxide: Enhanced photocatalytic activity for hydrogen generation from water显示文摘 | Rajamma Sasikala Archana P. Gaikwad Vasanthakumaran Sudarsan Nidhi Gupta Shyamala R. Bharadwaj | 2013 | Applied Catalysis A, General2013，，： | 1 |
| 17 | Biology of spiralling whitefly, A leurodicus dispersus Russell ( Homoptera: Aleyrodidae) 显示文摘 | Rajamma P Rajasrcc K M Jayaprakas C A | 2002 | Journal of Root Crops2002，28，1： | 1 |
| 18 | Characterisation and Use of Biomass Fy Ash in Cement-based Materials显示文摘 | Rajamma R Ball R J Tarelho L A C | 2009 | Journal of Hazardous Materials2009，172，： | 1 |
| 19 | Lipoma causing Guyon’s canal syndrome: a case report and review显示文摘Compression of the ulnar nerve in Guyon’s canal leads to Guyon’s canal syndrome.Lipoma is a rare cause of such compressions with only 12 cases reported previously.We report a 55-year-old man who presented with swelling in the left hand with decreased sensation in the ring and littlefingers.Magnetic resonance imaging revealed high signals in T1-weighted and T2-weighted images with suppression of the short T1 inversion recovery signal,suggestive of lipoma.On exploration a well-encapsulated,dumbbell-shaped,fatty tumor was seen in the hypothenar space and Guyon’s canal.The tumor was enucleated in toto.At 6-month follow-up,the patient had fully regained sensation.A review of the literature is presented for similar cases where a lipoma was the cause of Guyon’s canal syndrome. | Narayanathu Chellappantilla Sreekumar Panambur Laxminarayan Bhandari Lalitha Sreedharan Sreelesh Krishnankutty Rajamma Thushara | 2014 | Plastic and Aesthetic Research2014，1，1： | 0 |
| 20 | Loss of cavin1 and expression of p-caveolin-1 in pulmonary hypertension: Possible role in neointima formation显示文摘BACKGROUND Pulmonary hypertension(PH) is a progressive disease with a high morbidity and mortality rate; and neointima formation leads to the irreversibility of the disease.We have previously reported that in rats, monocrotaline(MCT) injection leads to progressive disruption of endothelial cells(EC), and endothelial caveolin-1(cav-1) loss, accompanied by the activation of pro-proliferative pathways leading to PH. Four weeks post-MCT, extensive endothelial cav-1 loss is associated with increased cav-1 expression in smooth muscle cells(SMC). Exposing the MCTtreated rats to hypoxia hastens the disease process; and at 4 wk, neointimal lesions and occlusion of the small arteries are observed.AIM To identify the alterations that occur during the progression of PH that lead to neointima formation.METHODS Male Sprague-Dawley rats(150-175 g) were divided in 4 groups(n = 6-8 per group): controls(C); MCT(M, a single sc injection 40 mg/kg); Hypoxia(H,hypobaric hypoxia); MCT + hypoxia(M+H, MCT-injected rats subjected to hypobaric hypoxia starting on day1). Four weeks later, right ventricular systolic pressure(RVSP), right ventricular hypertrophy(RVH), lung histology, and cav-1 localization using immunofluorescence technique were analyzed. In addition, the expression of cav-1, tyrosine 14 phosphorylated cav-1(p-cav-1), caveolin-2(cav-2), cavin-1, vascular endothelial cadherin(VE-Cad) and p-ERK1/2 in the lungs were examined, and the results were compared with the controls.RESULTSSignificant PH and right ventricular hypertrophy were present in M and H groups [RVSP, mmHg, M 54±5~*, H 45±2~*, vs C 20±1, P < 0.05; RVH, RV/LV ratio M 0.57±0.02~*, H 0.50±0.03~*, vs C 0.23±0.007, P < 0.05]; with a further increase in M+H group [RVSP 69±9 mmHg, RV/LV 0.59±0.01 P < 0.05 vs M and H]. All experimental groups revealed medial hypertrophy; but only M+H group exhibited small occluded arteries and neointimal lesions. Immunofluorescence studies revealed endothelial cav-1 loss and increased cav-1 expression in SMC in M group; however, the total cav-1 level in the lungs remained low. In the M+H group, significant endothelial cav-1 loss was associated with increasing expression of cav-1 in SMC; resulting in near normalization of cav-1 levels in the lungs [cav-1, expressed as % control, C 100±0, M 22±4~*, H 96±7, M+H 77±6, ~* = P< 0.05 vs C]. The expression of p-cav-1 was observed in M and M+H groups [M314±4%, M+H 255±22% P < 0.05 vs C]. Significant loss of cav-2 [% control, C100±0, M 15±1.4~*, H 97±7, M+H 15±2~*; M and M+H vs C, ~* = P < 0.05], cavin-1 [%control, C 100±0, M 20±3~*, H 117±7, M+H 20±4~*; M and M+H vs C, P < 0.05] and VE-Cad [% control, C 100±0, M 17±4~*, H 96±9, M+H 8±3~*; M and M+H vs C, P <0.05] was present in M and M+H groups, confirming extensive disruption of EC.Hypoxia alone did not alter the expression of cav-1 or cav-1 related proteins.Expression of p-ERK1/2 was increased in all 3 PH groups [%control, C 100±0, M284±23~*, H 254±25~*, M+H 270±17~*; ~* = P < 0.05 vs C].CONCLUSION Both cavin-1 loss and p-cav-1 expression are known to facilitate cell migration;thus, these alterations may in part play a role in neointima formation in PH. | Jing Huang Rajamma Mathew | 2019 | World Journal of Hypertension2019，9，2： | 0 |
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