Search

Your search keyword '"Ahuja, Nancy"' showing total 15 results
Start Over Author "Ahuja, Nancy"
15 results on '"Ahuja, Nancy"'

5. Vitamin D3-VDR-PTPN6 axis mediated autophagy contributes to the inhibition of macrophage foam cell formation

Author

Kumar, Sumit, primary, Nanduri, Ravikanth, additional, Bhagyaraj, Ella, additional, Kalra, Rashi, additional, Ahuja, Nancy, additional, Chacko, Anuja P., additional, Tiwari, Drishti, additional, Sethi, Kanupriya, additional, Saini, Ankita, additional, Chandra, Vemika, additional, Jain, Monika, additional, Gupta, Shalini, additional, Bhatt, Deepak, additional, and Gupta, Pawan, additional

Published
2020
Full Text
View/download PDF

6. Vitamin D3-VDR-PTPN6 axis mediated autophagy contributes to the inhibition of macrophage foam cell formation.

Author

Kumar, Sumit, Nanduri, Ravikanth, Bhagyaraj, Ella, Kalra, Rashi, Ahuja, Nancy, Chacko, Anuja P., Tiwari, Drishti, Sethi, Kanupriya, Saini, Ankita, Chandra, Vemika, Jain, Monika, Gupta, Shalini, Bhatt, Deepak, and Gupta, Pawan

Subjects
RETINOID X receptors, AUTOPHAGY, VITAMIN D receptors, MITOGEN-activated protein kinases, FOAM cells
Abstract

Macrophage derived foam cells in atherosclerotic plaques are the major factor responsible for the pathogenesis of atherosclerosis (AS). During advanced AS, macrophage-specific macroautophagy/autophagy is dysfunctional. 1, 25-dihydroxy vitamin D3 (VitD3) and its receptor VDR (vitamin D receptor) are reported to inhibit foam cell formation and induce autophagy; however, the role of VitD3-VDR-induced autophagy and foam cell formation in AS has not been explored. Here we find that VitD3 significantly recovered oxidized low-density lipoprotein-impaired autophagy, as well as increased autophagy-mediated lipid breakdown in mouse bone marrow-derived macrophages and human monocyte-derived macrophages, thus inhibiting the conversion of macrophages into foam cells. Importantly, VitD3 functions through its receptor VDR to upregulate autophagy and attenuate the accumulation of lipids in macrophages. Moreover, this study is the first occasion to report the interesting link between VitD3 signaling and PTPN6/SHP-1 (protein tyrosine phosphatase non-receptor type 6) in macrophages. VitD3-induced autophagy was abrogated in the presence of the PTPN6/Ptpn6 shRNA or inhibitor. VDR along with RXRA (retinoid X receptor alpha), and NCOA1 (nuclear receptor coactivator 1), are recruited to a specific response element located on the gene promoter and induce PTPN6 expression. PTPN6 contributes to VitD3-mediated autophagy by regulating autophagy-related genes via activation of MAPK1 (mitogen-activated protein kinase 1) and CEBPB (CCAAT enhancer binding protein beta). Furthermore, expression of PTPN6 is also crucial for VitD3-mediated inhibition of macrophage foam cell formation through autophagy. Thus, VitD3-VDR-PTPN6 axis-regulated autophagy attenuates foam cell formation in macrophages. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

7. NR1D1 ameliorates Mycobacterium tuberculosis clearance through regulation of autophagy

Author

Bhagyaraj, Ella, Ravikanth Nanduri, Gupta, Pawan, Vemika Chandra, and Ahuja, Nancy

Abstract

NR1D1 (nuclear receptor subfamily 1, group D, member 1), an adopted orphan nuclear receptor, is widely known to orchestrate the expression of genes involved in various biological processes such as adipogenesis, skeletal muscle differentiation, and lipid and glucose metabolism. Emerging evidence suggests that various members of the nuclear receptor superfamily perform a decisive role in the modulation of autophagy. Recently, NR1D1 has been implicated in augmenting the antimycobacterial properties of macrophages and providing protection against Mycobacterium tuberculosis infection by downregulating the expression of the IL10 gene in human macrophages. This antiinfective property of NR1D1 suggests the need for an improved understanding of its role in other host-associated antimycobacterial pathways. The results presented here demonstrate that in human macrophages either ectopic expression of NR1D1 or treatment with its agonist, GSK4112, enhanced the number of acidic vacuoles as well as the level of MAP1LC3-II, a signature molecule for determination of autophagy progression, in a concentration- and time- dependent manner. Conversely, a decrease in NR1D1 in knockdown cells resulted in the reduced expression of lysosomal-associated membrane protein 1, LAMP1, commensurate with a decrease in the level of transcription factor EB, TFEB. This is indicative of that NR1D1 may have a regulatory role in lysosome biogenesis. NR1D1 being a repressor, its positive regulation on LAMP1 and TFEB is suggestive of an indirect byzantine mechanism of action. Its role in the modulation of autophagy and lysosome biogenesis together with its ability to repress IL10 gene expression supports the theory that NR1D1 has a pivotal antimycobacterial function in human macrophages.

Published
2018
Full Text
View/download PDF

15. NR1D1 ameliorates Mycobacterium tuberculosisclearance through regulation of autophagy

Author

Chandra, Vemika, Bhagyaraj, Ella, Nanduri, Ravikanth, Ahuja, Nancy, and Gupta, Pawan

Abstract

NR1D1 (nuclear receptor subfamily 1, group D, member 1), an adopted orphan nuclear receptor, is widely known to orchestrate the expression of genes involved in various biological processes such as adipogenesis, skeletal muscle differentiation, and lipid and glucose metabolism. Emerging evidence suggests that various members of the nuclear receptor superfamily perform a decisive role in the modulation of autophagy. Recently, NR1D1 has been implicated in augmenting the antimycobacterial properties of macrophages and providing protection against Mycobacterium tuberculosisinfection by downregulating the expression of the IL10gene in human macrophages. This antiinfective property of NR1D1 suggests the need for an improved understanding of its role in other host-associated antimycobacterial pathways. The results presented here demonstrate that in human macrophages either ectopic expression of NR1D1 or treatment with its agonist, GSK4112, enhanced the number of acidic vacuoles as well as the level of MAP1LC3-II, a signature molecule for determination of autophagy progression, in a concentration- and time-dependent manner. Conversely, a decrease in NR1D1 in knockdown cells resulted in the reduced expression of lysosomal-associated membrane protein 1, LAMP1, commensurate with a decrease in the level of transcription factor EB, TFEB. This is indicative of that NR1D1 may have a regulatory role in lysosome biogenesis. NR1D1 being a repressor, its positive regulation on LAMP1 and TFEB is suggestive of an indirect byzantine mechanism of action. Its role in the modulation of autophagy and lysosome biogenesis together with its ability to repress IL10gene expression supports the theory that NR1D1 has a pivotal antimycobacterial function in human macrophages.

Published
2015
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results