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Nephrin and Podocalyxin - New Podocyte Proteins for Early Detection of Secondary Nephropathies

domainmediated interaction of rabbit podocalyxin and Na+/H+ exchange regulatory factor-2. Am J Physiol Renal Physiol 2002; 282(6): F1129-F1139. 17. Doyonnas DB Kershaw, Duhme C, et al. Anuria, omphalocele, and perinatal lethality in mice lacking the CD34- related protein podocalyxin. J Exp Med 2001; 194(1): 13-27. 18. Takeda T, Go WY, Orlando RA, et al. Expression of podocalyxin inhibits cell-cell adhesion and modifies junctional properties in Madin-Darby canine kidney cells. Mol Biol Cell 2000; (11): 3219-3232. 19. Pollak MR

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Podocytes and Proteinuric Kidney Disease

(Bethesda) 2009; 24: 88-96. 13. Abbate M Zoja C, Morigi M, et al. Transforming growth factor-beta1 is upregulated by podocytes in response to excess intraglomerular passage of proteins. A central pathway in progressive glomerulosclerosis. Am J Path 2002; 161: 2179. 14. Benzing T. Signaling at the slit diaphragm. J Am Soc Nephrol 2004; 15: 1382-1391. 15. Lasagni L, Romagnani P. Glomerular epithelial stem cells, the good, the bad, and the ugly. J Am Soc Nephrol 2010; 21: 1612-1619. 16. Welsh GI, Saleem MA. The podocyte cytoskeleton-key to a functioning

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Aplastic anemia in China

(CSA)], the cytotoxicity of CD 8 + HLA-DR + T cells was reduced and then reached the normal state. Moreover, the expression of perforin, [ 4 ] granular enzyme, TNF-β, and FasL, as well as many other hematopoietic negative regulatory factors, were elevated obviously in these effector T cells in patients with AA, [ 5 ] suggesting that hematopoietic stem and progenitor cells might be destroyed through lymphokine-induced apoptosis. [ 6 ] Particularly worth mentioning is the expression of linker for activation of T cells (LAT) in CD3 + T cells was positively

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Shear stress regulation of endothelium: A double-edged sword

-like factor 4 protects against atherothrombosis in mice J Clin Invest 2012 122 4727 31 12 Yoshida T, Yamashita M, Horimai C, Hayashi M. Deletion of Kruppel-Like Factor 4 in Endothelial and Hematopoietic Cells Enhances Neointimal Formation Following Vascular Injury. J Am Heart Assoc 2014; 3:e000622. Yoshida T Yamashita M Horimai C Hayashi M. Deletion of Kruppel-Like Factor 4 in Endothelial and Hematopoietic Cells Enhances Neointimal Formation Following Vascular Injury J Am Heart Assoc 2014 3 e000622 13 Shen B, Smith RS, Hsu YT, Chao L, Chao J. Kruppel-like Factor 4 Is a

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Current status and inspiration on macrolides in the treatment of chronic obstructive pulmonary disease

-72. 4. Bai J, Qiu SL, Zhong XN, Huang QP, He ZY, Zhang JQ, et al. Erythromycin enhances CD4+Foxp3+ regulatory T-cell responses in a rat model of smoke-induced lung inflammation. Mediators Inflamm 2012; 2012: 410232. 5. He Z, Li B, Yu L, Liu Q, Zhong N, Ran P. Suppression of oxidantinduced glutathione synthesis by erythromycin in human bronchial epithelial cells. Respiration 2008; 75: 202-9. 6. Zhong XN, Guo SM. An experimental study on pulmonary vascular inflammation in a rat model of chronic bronchitis and emphysema. Chin J Tuberc

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2016 Revision to the WHO classification of acute myeloid leukemia

right stage of differentiation for subsequent malignant transformation. Notably, GATA2 expression levels in primary inv(3)/t(3;3) AML cases and cell lines ( n =78) were found to be significantly reduced as compared to controls (213 AML patients). In addition, monoallelic GATA2 expression was found as a consequence of GATA2 inactivation on the rearranged allele in cases with inv(3) or t(3;3). Thus, the inversion/translocation event in inv(3)/t(3;3) malignancies reorganizes an originally upstream regulatory element of the GATA2 domain, causing reduced and functional

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The role of heat shock proteins in kidney disease

and worse survival following renal IRI. The protective effect from renal IRI provided by the HSP 70 inducing agent geranylgeranylacetone is also abrogated in HSP 70 knockout mice. The main barrier to the translation of these treatments to clinical use is the lack of complete understanding how HSP 70 induction results in kidney protection. The putative modes of protection include cytoskeletal stabilization, anti-inflammatory effects, requirement in autophagy, anti-apoptotic properties, influence over macrophage phenotype and stimulation of regulatory T cells. In

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MicroRNA regulated macrophage activation in obesity

by targeting key regulators. PPARγ directly binds upstream of miR-223 and mediates anti-inflammatory signaling by inhibiting the expression of Nuclear Factor of Activated T-Cells 5 (NFATt5) and RAS p21 Protein Activator 1 (RASA1), thereby promoting “M2-like” activation. Deletion of miR-223 can abolish PPARγ-regulated M2 activation of murine macrophages in vivo and ex vivo .[ 63 ] In addition, miR-223 inhibits the expression of PBX/Knotted 1 Homeobox 1 (Pknox1), thus suppressing NFκB/JNK signaling and “M1-like” pro-inflammation activation.[ 64 ] miR-223 also

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Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis

. investigated the regulatory role of hypoxia on endosialin expression. It showed that CD248/endosialin mRNA and protein levels in human cell lines were significantly higher in hypoxic conditions than normoxic conditions.[ 33 ] HIF-2 alpha binds hypoxia-responsive element at position–976/–969, thereby regulating the endosialin promoter and hypoxic induction of endosialin. Hypothesis Based on the existing knowledge, we hypothesize that hypoxia microenvironment induced by BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then

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Importance of studying the levels of hepcidin and vitamin D in Egyptian children with chronic hepatitis C

various diseases are still deficient and contradictory. Vitamin D plays a significant role in the inflammatory responses and fibrosis in HCV infection. [ 11 ] It is a powerful immunomodulator, suppressing proinflammatory cytokines, increasing anti-inflammatory cytokines, and improving CD4 T-cell responsiveness. Vitamin D status is influenced by exposure to sunlight so it differs across different environmental and geographical locations, and consequently, its effect on disease pathogenesis varies from one place to the other. [ 12 ] This study was carried out on

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