Ghosh-Choudhury, NandiniGraduate School of Biomedical Sciences |
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| 9/2006 - Present | Professor of Research & Principal Investigator | The University of Texas Health Science Center, Pathology, San Antonio, TX |
| 8/2002 - Present | Research Health Scientist | South Texas Veterans Health Care System, San Antonio, TX |
| Year | Degree | Discipline | Institution |
| 1990 | PhD | Biochemistry | McMaster University Ontario , Canada |
| 1978 | MS | Biochemistry (Ranked second in class) | University of Calcutta Calcutta , India |
| 1976 | BS | Chemistry (Honors), Physics, Mathematics | University of Calcutta Calcutta , India |
| Postdoctoral Training | Dept. of Medicine, Division of Endocrinology | The University of Texas Health Science Center San Antonio , TX |
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| Postdoctoral Fellowship | Cellular & Structural Biology | The University of Texas Health Science Center San Antonio , TX |
Bone Biology, Breast Cancer, Signal Transduction- Mechanism of signal transduction by Bone Morphogenetic Protein-2 (BMP-2) in osteoblast and cardiomyocyte differentiation; osteoporosis; bone metastasis of breast cancer |
Personal Statement- My research is focused on elucidating the mechanism of bone remodeling and bone regeneration following age- and disease-induced fracture healing. We investigate the mechanism of BMP-2-induced active osteoclast formation, a fairly new concept with very limited available mechanistic details. We defined a novel signal transduction pathway involving c-Abl tyrosine kinase in BMP-2-mediated gene expression leading to osteoclast formation. I have over ten years experience in conducting research involving BMP-2 gene regulation and related signal transduction pathways. My research group pioneered the discovery of the involvement of PI 3 kinase/Akt signaling and its crosstalk with Smad signaling pathway during BMP-2-induced osteoblast and osteoclast activation. We were one of the first groups to report the essential involvement of BMP-2 in osteoclast differentiation and the very first to identify BMP-2-induced CSF-1 gene expression to be the underlying mechanism for this critical biological event. I published many relevant peer reviewed publications as a senior author in this field of research and I have close collaborations with other leaders in this field. My research is also directed to elucidate the mechanism of breast cancer growth and subsequent bone metastasis. We investigate the mechanism of inhibition of active osteoclast formation and breast cancer cell migration by omega-3 fatty acids and statin group of drugs. We defined a novel mechanism of action for the omega-3 fatty acids regulating microRNA expression to increase tumor suppressor gene expression that in turn has the ability to block breast cancer growth and metastasis. We also pioneered in deciphering a novel role of statins in upregulating expressions of tumor suppressor proteins, p53 and PTEN and in suppressing NFkB activity resulting in decreased expression of antiapoptotic protein, BclXL. We describe a new role of statins in inhibiting breast cancer bone metastasis by interfering with the prometastatic CD44 expression through p53-mediated transcriptional pathway. We are actively working to establish alternative non-toxic therapeutical pathways to control breast tumor growth and metastasis by statins and w-3 fatty acid combinations added to a lower dose of the conventional therapy regimes to nullify their deleterious side effects. |
| Date | Description | Institution | # Students |
| 8/2009 - Present | Graduate Student Advisor for the Cancer Biology Track | The University of Texas Health Science Center | |
| 1/2008 - Present | Core Course III/Cell Biology | The University of Texas Health Science Center | 6 students |
| 3/2006 - Present | Post-Doctoral Student Supervision | The University of Texas Health Science Center at San Antonio, TX | |
| 1/2005 - Present | Post-Doctoral Student Supervision | University of Texas Health Science Center at San Antonio, TX | |
| 1/2003 - Present | Post-Doctoral Student Supervision | The University of Texas Health Science Center at San Antonio, TX | |
Abstract |
| Das F, Bera A, Ghosh-Choudhury N, Mariappan MM, Kasinath BS, Ghosh-Choudhury G. Hydrophobic motif site phosphorylation of protein kinase C beta II by mTORC2 regulates high glucose-induced mesangial cell hypertrophy; 2015 Jan. (J Am Soc Nephrol; vol. Suppl, no. 26). |
| Bera A, Das F, Ghosh-Choudhury N, Kasinath BS, Abboud HE, Ghosh-Choudhury G. Rictor-PDED4 interaction controlled by microRNA 21 contributes to renal cancer cell invasion; 2014 Jan. (J Am Soc Nephrol; vol. 25). |
| Das F, Bera A, Ghosh-Choudhury N, Abboud HE, Kasinath BS, Ghosh-Choudhury G. mTOR component deptor contributes to TGFbeta induced collagen I alpha2 expression in proximal tubular epithelial cells; 2014 Jan. (J Am Soc Nephrol; vol. 25). |
| Bera A, Das F, Mariappan MM, Ghosh-Choudhury N, Kasinath BS, Ghosh-Choudhury G. microRNA-214 regulates mesangial cell (MC) hypertrophy and matrix expansion through PTEN; 2013 Jan. (J Am Soc Nephrol). |
| Das F, Bera A, Ghosh-Choudhury N, Kasinath BS, Abboud HE, Ghosh-Choudhury G. PDGF launches mesangial cell proliferation via a positive feedback loop involving EKK5 and Akt downstream of PI kinase; 2013 Jan. (J Am Soc Nephrol). |
| Bera A, Dey N, Das F, Kasinath BS, Abboud HE, Ghosh-Choudhury N, Ghosh-Choudhury G. microRNA-21-dependent positive feedback loop involving NFkappaB (NFkB) regulates renal cancer cell proliferation; 2012 Dec. (J Am Soc Nephrol; vol. 23). |
| Das F, Ghosh-Choudhury N, Dey N, Abboud HE, Kasinath BS, Ghosh-Choudhury G. A signal relay from transforming growth factor beta (TGFb)-stimulated Smad 3 to mTOR involves deptor suppression to force mesangial cell hypertrophy; 2012 Nov. (J Am Soc Nephrol; vol. 23). |
| Mahimainathan L, Das F, Ghosh-Choudhury N, Gorin Y, Kasinath BS, Abboud HE, Ghosh-Choudhury G. A Cross talk between two small GTPases Rac1 and Rheb regulates IGF-1-induced protein synthesis in mesangial cell (MC). [SA-PO788]; 2006 Jan. (J Am Soc Nephrol). |
| Ghosh-Choudhury G, Ghosh-Choudhury N, Mahimainathan L, Das, F. Transforming growth factor-beta (TGF β) ?stimulated PI 3 kinase/Akt signaling targets Smad3 transactivation for PAI-1 gene expression in mesangial cell (MC); 2006 Jan. (J Am Soc Nephrol). |
| Mahimainathan L, Ghosh-Choudhury N, Gorin Y, Mummidi S, Kasinath BS, Abboud HE, Ghosh-Choudhury G. Rheb trafficks IGF-1 signals in renal cells: Role of reactive oxygen species (ROS). (Abstract SA- PO177); 2005 Jan. (J Am Soc Nephrol; vol. 16). |
| Ghosh-Choudhury N, Chandrasekar B, Abboud SL, Ghosh-Choudhury G. BMP-2 controls cardiomyocyte contractility by activating phosphatidylinositol 3 kinase signaling pathway; 2003 Jan. (J Bone Miner Res; vol. 18, no. supp2). |
| Ghosh-Choudhury N, Abboud SL, Ghosh-Choudhury G. BMP-2-induced phosphatidylinositol 3 kinase (PI 3-K) regulates GATA-4 and MEF-2 transcription factors during cardiomyocyte differentiation; 2002 Jan. (J Bone Miner Res; vol. 17). |
| Ghosh-Choudhury N, Abboud SL, Ghosh-Choudhury G. Phosphatidylinositol 3 kinase (PI 3-K) and Akt serine/threonine kinase regulate BMP-2 induced osteoblast differentiation and Smad-dependent transcription of BMP-2 gene; 2001 Jan. (J Bone Miner Res; vol. 16). |
| Ghosh-Choudhury N, Ghosh-Choudhury G, Woodruff KA, Bsoul S, Nishimura R, Qi W, Celeste A, Abboud SL. Identification of a smad-binding element (SBE) in BMP-2 responsive CSF-1 gene promoter: a mechanism of BMP-2-mediated transregulation of osteoclastogenesis during bone remodeling; 2000 Jan. (J Bone Miner Res; vol. 15). |
| Ghosh-Choudhury G, Jin D-C, Kim Y-S, Celeste A, Ghosh-Choudhury N, Abboud HE. Bone morphogenetic protein 2 (BMP-2) inhibits EGF-induced DNA synthesis in mesangial cells (MC) via blocking MAPK-dependent Elk-1 transactivation and by increasing p21 cyclin kinase inhibitor transcription respectively; 1999 Jan. (J Am Soc Nephrol; vol. 10). |
| Ghosh-Choudhury N, Ghosh-Choudhury G, Besoul S, Woodruff KA, Abboud SL. Regulation of CSF-1 gene transcription by BMP-2 during osteoblast differentiation: Mapping of BMP-2 responsive element; 1999 Jan. (J Bone Miner Res; vol. 14). |
| Ghosh-Choudhury N, Celeste A, Harris SE, Ghosh-Choudhury G. Bone morphogenetic protein 2 (BMP-2)-induced osteoblast cell proliferation is mediated by mitogen-activated protein kinase (MAPK)-dependent c-fos gene transcription; 1998 Jan. (Bone; vol. 22). |
| Ghosh-Choudhury N, Ghosh-Choudhury G, Celeste A., Ghosh P, Stapleton M., Kreisberg J. Bone morphogenetic protein 2 blocks estrogen-induced human breast cancer cell growth by intercepting mitogen activated protein kinase (MAPK)-dependent nuclear signals; 1998 Jan. (Bone; vol. 22). |
Journal Article |
| Maity S, Bera A, Ghosh-Choudhury N, Das F, Kasinath BS, Choudhury GG. microRNA-181a downregulates deptor for TGF?-induced glomerular mesangial cell hypertrophy and matrix protein expression 2018 Mar;364. |
| Ghosh-Choudhury N. Tyrosines-740/751 of PDGFRβ contribute to the activation of Akt/Hif1α/TGFβ nexus to drive high glucose-induced glomerular mesangial cell hypertrophy 2018 Jan;42. |
| Bera A, Das F, Ghosh-Choudhury N, Mariappan MM, Kasinath BS, Ghosh Choudhury G. Reciprocal regulation of miR-214 and PTEN by high glucose regulates renal glomerular mesangial and proximal tubular epithelial cell hypertrophy and matrix expansion 2017 Oct;1:C430-C447. |
| Das F, Dey N, Bera A, Kasinath BS, Ghosh-Choudhury N, Choudhury GG. MicroRNA-214 Reduces Insulin-like Growth Factor-1 (IGF-1) Receptor Expression and Downstream mTORC1 Signaling in Renal Carcinoma Cells 2016 Jul;28:14662-14676. |
| Das F, Dey N, Bera A, Ghosh-Choudhury N, Kasinath BS, Ghosh-Choudhury G. microRNA 214 Reduces IGF-1 Receptor Expression and Downstream mTORC1 signaling in renal carcinoma cells J Biol Chem 2016 Jan;291:14662-14676. |
| Mandal CC, Das F, Ganapathy S, Harris SE, Ghosh-Choudhury G, Ghosh-Choudhury N. Bone Morphogenetic Protein-2 (BMP-2) Activates NFATc1 Transcription Factor via an Autoregulatory Loop Involving Smad/Akt/Ca2 Signaling J Biol Chem 2016 Jan;291:1148-1161. |
| Das F, Ghosh-Choudhury N, Mariappan MM, Kasinath BS, Ghosh-Choudhury G. Hydrophobic Motif Site-phosphorylated Protein Kinase CβII between mTORC2 and Akt Regulates High Glucose-induced Mesangial Cell Hypertrophy Am J Physiol Cell Physiol 2016 Jan;310(7):C583-C596. |
| Bera A, Das F, Ghosh-Choudhury N, Li X, Pal S, Gorin Y, Kasinath BS, Abboud HE, Ghosh-Choudhury G. A positive feedback loop involving Erk5 and Akt turns on mesangial cell proliferation in response to PDGF Am J Physiol Cell Physiol 2014 Jun;306(11):C1089-C1100. |
| Bera A, Das F, Ghosh-Choudhury N, Kasinath BS, Abboud HE, Ghosh-Choudhury G. microRNA-21-induced dissociation of PDCD4 from rictor contributes to Akt-IKKβ-mTORC1 axis to regulate renal cancer cell invasion Exp Cell Res 2014 Jan;328(1):99-117. |
| Das F, Bera A, Ghosh-Choudhury N, Abboud HE, Kasinath BS, Ghosh-Choudhury G. TGFβ-Induced Deptor Suppression Recruits mTORC1 and Not mTORC2 to Enhance Collagen I (α2) Gene Expression PLoS One 2014 Jan;9(10). |
| Das F, Ghosh-Choudhury N, Dey N, Bera A, Mariappan MM, Kasinath BS, Ghosh-Choudhury G. High Glucose Forces a Positive Feed Back Loop Connecting Akt Kinase and FoxO1 to Activate mTORC1 for Mesangial Cell Hypertrophy and Matrix Protein Expression J Biol Chem 2014 Jan;289:32703-32716. |
| Bera, Ghosh-Choudhury N, Dey N, Das F, Kasinath BS, Abboud HE, Choudhury GG. NFkB-Mediated Cyclin D1 Expression By microRNA-21 Influences Renal Cancer Cell Proliferation Cell Signal 2013 Dec;25(12):2575-2586. |
| Ghosh-Choudhury N, Mandal CC, Das F, Ganapathy S, Ahuja SS, Ghosh-Choudhury G. c-Abl-dependent molecular circuitry involving Smad5 and phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2-induced osteogenesis J Biol Chem 2013 Aug;288(34):24503-24517. |
| Das F, Ghosh-Choudhury N, Bera A, Kasinath BS, Ghosh-Choudhury G. TGF Beta-induced PI 3 kinase-dependent Mnk-1 activation is necessary for Ser-209 phosphorylation of eIF4E and mesangial cell hypertrophy Journal of Cell Physiology 2013 Jul;228(7):1617-1626. |
| Das Falguni, Ghosh-Choudhury N, Bera Amit, Dey N, Abboud HE, Kasinath BS, Ghosh-Choudhury G. TGF beta integrates SMAD 3 to mechanistic target of rapamycin complexes to arrest deptor abundance for glomerular mesangial cell hypertrophy J Biol Chem 2013 Mar;288(11):7756-7768. |
| Das F, Ghosh-Choudhury N, Bera A, Dey N, Abboud HE, Kasinath BS, Ghosh-Choudhury G. Transforming Growth Factor ? Integrates Smad 3 to Mechanistic Target of Rapamycin Complexes to Arrest Deptor Abundance for Glomerular Mesangial Cell Hypertrophy Journal of Biological Chemistry 2013 Feb;288:7756-7768. |
| Das F, Ghosh-Choudhury N, Bera A, Dey N, Abboud HE, Kasinath BS, Ghosh Choudhury G. TGF? integrates SMAD 3 to mechanistic target of rapamycin complexes to arrest deptor abundance for glomerular mesangial cell hypertrophy J Biol Chem 2013 Jan;288(11):7756-7768. |
| Das F, Ghosh-Choudhury N, Bera A, Kasinath BS, Choudhury GG. TGF?-induced PI 3 kinase-dependent MNK-1 activation is necessary for Ser-209 phosphorylation of eIF4E and mesangial cell hypertrophy J Cell Physiol [Epub ahead of print] 2013 Jan;. |