Dr Sampath( Sampathkumar) Rangasamy, PhD - Translational Genomics Research Institute - Research Assistant Professor

Dr Sampath( Sampathkumar) Rangasamy

PhD

Translational Genomics Research Institute

Research Assistant Professor

Phoenix, AZ | USA

ORCID logohttps://orcid.org/0000-0003-2151-9162

Dr Sampath( Sampathkumar) Rangasamy, PhD - Translational Genomics Research Institute - Research Assistant Professor

Dr Sampath( Sampathkumar) Rangasamy

PhD

Introduction

Primary Affiliation: Translational Genomics Research Institute - Phoenix, AZ , USA

Education

Aug 2002 - Aug 2008
University of Madras
PhD-Biochemistry and Cell Biology
Madras Diabetes Research FOundation
Aug 1996 - Jun 1998
Bharathidasan University
MSc-Applied Microbiology
National Facility for Marine Cyanobacteria and Department of Microbiology
Aug 1992 - Jun 1996
Bharathiar University
B.Sc
Biochemistry

Experience

Aug 2014 - Nov 2014
Translational Genomics Research Institute (TGen)
Research Assistant Professor
Genomics, Neurogenetics and Cell Biology
Apr 2012 - Jan 2014
Barrow Neurological Institute
Senior Post Doctoral Fellow
Developmental Neurogenetics Laboratory
Aug 2008 - Aug 2008
University of New Mexico School of Medicine
Post Doctoral Fellow
Cell Biology and Biochemistry
Aug 2001 - Aug 2001
Madras Diabetes Research Foundation
Research Fellow
Cell Biology and Biochemistry
Dec 2006
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Publications

31Publications

677Reads

97Profile Views

395PubMed Central Citations

Do Genomic Factors Play a Role in Diabetic Retinopathy?

J Clin Med 2020 Jan 14;9(1). Epub 2020 Jan 14.

Department of Surgery/Ophthalmology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.

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http://dx.doi.org/10.3390/jcm9010216DOI Listing
January 2020

Rare De Novo Missense Variants in RNA Helicase DDX6 Cause Intellectual Disability and Dysmorphic Features and Lead to P-Body Defects and RNA Dysregulation.

Am J Hum Genet 2019 Sep 15;105(3):509-525. Epub 2019 Aug 15.

Institute of Genetics and Molecular and Cellular Biology, Illkirch, France; French National Center for Scientific Research, UMR7104, 67400 Illkirch, France; National Institute of Health and Medical Research U964, 67400 Illkirch, France; University of Strasbourg, 67081 Illkirch, France; Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH 44195, USA. Electronic address:

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https://linkinghub.elsevier.com/retrieve/pii/S00029297193027
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http://dx.doi.org/10.1016/j.ajhg.2019.07.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6731366PMC
September 2019
4 Reads
10.931 Impact Factor

Neonatal epileptic encephalopathy caused by de novo GNAO1 mutation misdiagnosed as atypical Rett syndrome: Cautions in interpretation of genomic test results.

Semin Pediatr Neurol 2018 07 16;26:28-32. Epub 2017 Aug 16.

Center for Rare Childhood Disorders, Translational Genomics Research Institute, Phoenix, AZ; Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ; School of Life Sciences, Arizona State University, Tempe, AZ. Electronic address:

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http://dx.doi.org/10.1016/j.spen.2017.08.008DOI Listing
July 2018
54 Reads
1.883 Impact Factor

Reduced neuronal size and mTOR pathway activity in the Mecp2 A140V Rett syndrome mouse model.

F1000Res 2016 8;5:2269. Epub 2016 Sep 8.

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, USA; Center for Rare Childhood Disorders, Translational Genomics Research Institute, Phoenix, USA; Barrow Neurological Institute, St.Joseph's Hospital and Medical Center, Phoenix, USA; School of Life Sciences, Arizona State University, Tempe, USA.

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http://dx.doi.org/10.12688/f1000research.8156.1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040159PMC
September 2016
3 Reads
2 Citations

Incontinentia pigmenti (Bloch-Sulzberger syndrome).

Handb Clin Neurol 2015 ;132:271-80

Neurology Research, Barrow Neurological Institute, Phoenix, AZ, USA; Center for Rare Childhood Disorders, Translational Genomics Research Institute, Phoenix, AZ, USA; Arizona Pediatric Neurology and Neurogenetics Associates, Phoenix, AZ, USA. Electronic address:

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http://bjo.bmj.com/content/71/8/629.full.pdf
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http://linkinghub.elsevier.com/retrieve/pii/B978044462702500
Publisher Site
http://dx.doi.org/10.1016/B978-0-444-62702-5.00020-2DOI Listing
August 2016
108 Reads

Case Report: Compound heterozygous nonsense mutations in TRMT10A are associated with microcephaly, delayed development, and periventricular white matter hyperintensities.

F1000Res 2015 28;4:912. Epub 2015 Sep 28.

Arizona Pediatric Neurology & Neurogenetics Associates, Phoenix, AZ, USA ; Barrow Neurological Institute, Phoenix, AZ, USA ; Center for Rare Childhood Disorders, Translational Genomics Research Institute, Phoenix, AZ, USA ; Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ, USA.

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http://dx.doi.org/10.12688/f1000research.7106.1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617320PMC
November 2015
48 Reads
4 Citations

Diabetic Macular Edema: Pathophysiology and Novel Therapeutic Targets.

Ophthalmology 2015 Jul 30;122(7):1375-94. Epub 2015 Apr 30.

T-Gen Institute, Phoenix, Arizona.

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http://dx.doi.org/10.1016/j.ophtha.2015.03.024DOI Listing
July 2015
33 Reads
37 Citations
6.135 Impact Factor

Chemokine mediated monocyte trafficking into the retina: role of inflammation in alteration of the blood-retinal barrier in diabetic retinopathy.

PLoS One 2014 20;9(10):e108508. Epub 2014 Oct 20.

Department of Surgery, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States of America; New Mexico VA Health Care System, Albuquerque, New Mexico, United States of America.

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0108508PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203688PMC
July 2015
192 Reads
29 Citations
3.234 Impact Factor

A De Novo Mutation in TEAD1 Causes Non-X-Linked Aicardi Syndrome.

Invest Ophthalmol Vis Sci 2015 Jun;56(6):3896-904

Dorrance Center for Rare Childhood Disorders, Translational Genomics Research Institute, Phoenix, Arizona, United States 2Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, United States.

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http://dx.doi.org/10.1167/iovs.14-16261DOI Listing
June 2015
38 Reads
5 Citations
3.404 Impact Factor

New treatments for diabetic retinopathy.

Diabetes Obes Metab 2015 Mar 6;17(3):219-30. Epub 2014 Oct 6.

Department of Surgery/Ophthalmology, University of New Mexico School of Medicine, Albuquerque, NM, USA; Department of Surgery, New Mexico VA Health Care System, Albuquerque, NM, USA.

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http://dx.doi.org/10.1111/dom.12384DOI Listing
March 2015
15 Reads
7 Citations
6.360 Impact Factor

Epigenetics, autism spectrum, and neurodevelopmental disorders.

Neurotherapeutics 2013 Oct;10(4):742-56

Developmental Neurogenetics Laboratory, Barrow Neurological Institute, Phoenix, AZ, 85013, USA.

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http://dx.doi.org/10.1007/s13311-013-0227-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805864PMC
October 2013
2 Reads
25 Citations

The role of monocyte subsets in myocutaneous revascularization.

J Surg Res 2013 Aug 6;183(2):963-75. Epub 2013 Mar 6.

Department of Surgery, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

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http://dx.doi.org/10.1016/j.jss.2013.02.019DOI Listing
August 2013
7 Reads
3 Citations
1.940 Impact Factor

Molecular intricacies and the role of ER stress in diabetes.

Exp Diabetes Res 2012 4;2012:958169. Epub 2012 Jun 4.

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http://dx.doi.org/10.1155/2012/958169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3373128PMC
October 2012
2 Reads
5 Citations
3.540 Impact Factor

Diabetic retinopathy and inflammation: novel therapeutic targets.

Middle East Afr J Ophthalmol 2012 Jan;19(1):52-9

Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, NM 87131.

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http://dx.doi.org/10.4103/0974-9233.92116DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277025PMC
January 2012
39 Reads
43 Citations

Pericyte-derived sphingosine 1-phosphate induces the expression of adhesion proteins and modulates the retinal endothelial cell barrier.

Arterioscler Thromb Vasc Biol 2011 Dec 22;31(12):e107-15. Epub 2011 Sep 22.

Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA.

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http://dx.doi.org/10.1161/ATVBAHA.111.235408DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3225006PMC
December 2011
6 Reads
9 Citations
6.000 Impact Factor

A potential role for angiopoietin 2 in the regulation of the blood-retinal barrier in diabetic retinopathy.

Invest Ophthalmol Vis Sci 2011 Jun 1;52(6):3784-91. Epub 2011 Jun 1.

Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.

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http://dx.doi.org/10.1167/iovs.10-6386DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109054PMC
June 2011
8 Reads
28 Citations
3.404 Impact Factor

Oxidative stress is independently associated with non-alcoholic fatty liver disease (NAFLD) in subjects with and without type 2 diabetes.

Clin Biochem 2010 Jul 14;43(10-11):815-21. Epub 2010 Apr 14.

Madras Diabetes Research Foundation, Gopalapuram, Chennai, India.

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http://dx.doi.org/10.1016/j.clinbiochem.2010.04.003DOI Listing
July 2010
5 Reads
27 Citations
2.230 Impact Factor

Association of leukocyte count with varying degrees of glucose intolerance in Asian Indians: the Chennai Urban Rural Epidemiology Study (CURES-26).

Metab Syndr Relat Disord 2009 Jun;7(3):205-10

Dr. Mohan's Diabetes Specialities Centre and Madras Diabetes Research Foundation, WHO Collaborating Centre for Noncommunicable Disease Prevention and Control, Gopalapuram, Chennai, India.

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http://dx.doi.org/10.1089/met.2008.0024DOI Listing
June 2009
8 Reads
5 Citations
1.920 Impact Factor

Association of leukocyte count and hsCRP with metabolic abnormalities in subjects with normal glucose tolerance (CURES - 64).

J Assoc Physicians India 2009 Jan;57:27-32

Madras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialities Centre, Gopalapuram, Chennai, India.

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http://www.japi.org/january_2009/O-3.pdf
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January 2009
6 Reads
2 Citations

A common nonsynonymous single nucleotide polymorphism in the SLC30A8 gene determines ZnT8 autoantibody specificity in type 1 diabetes.

Diabetes 2008 Oct 30;57(10):2693-7. Epub 2008 Jun 30.

Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado, USA.

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http://dx.doi.org/10.2337/db08-0522DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551679PMC
October 2008
5 Reads
57 Citations
8.100 Impact Factor

Advanced glycation index and its association with severity of diabetic retinopathy in type 2 diabetic subjects.

J Diabetes Complications 2008 Jul-Aug;22(4):261-6. Epub 2008 Apr 16.

Madras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialities Center, Gopalapuram, Chennai, India.

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http://dx.doi.org/10.1016/j.jdiacomp.2007.05.005DOI Listing
August 2008
1 Read
4 Citations
1.925 Impact Factor

Glutamine fructose-6-phosphate amidotransferase (GFAT) gene expression and activity in patients with type 2 diabetes: inter-relationships with hyperglycaemia and oxidative stress.

Clin Biochem 2007 Sep 24;40(13-14):952-7. Epub 2007 May 24.

Madras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialties Center 6B, Conran Smith Road, Gopalapuram, Chennai, India.

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http://dx.doi.org/10.1016/j.clinbiochem.2007.05.002DOI Listing
September 2007
7 Citations
2.230 Impact Factor

Association of hypoglutathionemia with reduced Na+/K+ ATPase activity in type 2 diabetes and microangiopathy.

Mol Cell Biochem 2006 Jan;282(1-2):169-76

Madras Diabetes Research Foundation and Dr. Mohans' M.V. Diabetes Specialities Centre, Chennai, India.

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http://dx.doi.org/10.1007/s11010-006-1740-9DOI Listing
January 2006
2 Reads
6 Citations
2.393 Impact Factor

Increased glutathionylated hemoglobin (HbSSG) in type 2 diabetes subjects with microangiopathy.

Clin Biochem 2005 Oct;38(10):892-9

Department of Cell and Molecular Biology, Madras Diabetes Research Foundation, 6B, Conran Smith Road, Gopalapuram, Chennai-600 086, India.

Objective: Protein glutathionylation is considered an important post-translational modification in the pathogenesis of complex diseases. The aim of this study was to examine whether hemoglobin (Hb) is modified by reduced glutathione (GSH) via oxidation of the thiol groups present in diabetes and its associated microangiopathy and to determine whether oxidative imbalance has any correlation with glutathionylated Hb (HbSSG) levels.

Methods: The study group consisted of a total of 130 subjects which included non-diabetic healthy control subjects (n = 30) and type 2 diabetic patients with (n = 53) and without (n = 47) microangiopathy. All subjects were assessed for glycemic and lipidemic status, while diabetic subjects were also assessed for the diagnosis of retinopathy and nephropathy. RBC lysates from all the subjects were analyzed by liquid chromatography/electrospray ionization-mass spectrometry (LC/ESI-MS) for HbSSG beta-globin chains. Levels of GSH and thiobarbituric acid substances (TBARS) levels were measured by spectrophotometric and fluorimetric methods, respectively.

Results: The positivity for HbSSG in diabetic subjects with microangiopathy was significantly higher (69%) compared to diabetics without microangiopathy (22%) and control subjects (14%). In univariate regression analysis, HbSSG levels were significantly associated with the duration of diabetes, HbA1c, and TBARS levels. GSH levels were negatively correlated (r = -0.57, P < 0.001) with HbSSG in diabetic subjects. A significant inverse correlation (r = -0.42, P < 0.001) between the GSH levels and HbA1c levels was also seen in diabetic subjects.

Conclusions: This is perhaps the largest LC-MS-based study to demonstrate that HbSSG levels are markedly increased in diabetic subjects with microangiopathy. Since diabetic subjects also exhibited increased lipid peroxidation and decreased GSH levels, it appears that enhanced oxidative stress may account for the increased HbSSG concentrations and altered reduction-oxidation (redox) signaling.

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http://dx.doi.org/10.1016/j.clinbiochem.2005.06.009DOI Listing
October 2005
4 Reads
63 Citations
2.430 Impact Factor

A novel advanced glycation index and its association with diabetes and microangiopathy.

Metabolism 2005 Aug;54(8):1002-7

Madras Diabetes Research Foundation, Chennai, India 600 086.

Formation of advanced glycation end products (AGEs) is an important mechanism by which chronic exposure to high glucose levels leads to vascular complications. Measurement of AGEs is hence of great importance for clinicians and researchers concerned with the management and prevention of diabetic vascular disease. The aim of this study was to evaluate a simple methodology to detect AGEs in the serum and to correlate their levels with diabetes and microangiopathy, specifically retinopathy and nephropathy. We studied 157 subjects, which included nondiabetic control subjects (n = 38), type 2 diabetic patients without microangiopathy (n = 65), and type 2 diabetic subjects with retinopathy (n = 29) or both retinopathy and nephropathy (n = 25). All subjects were assessed for their glycemic and lipid status. Serum AGEs were monitored by recording the Maillard-specific fluorescence that resulted from sequential addition of serum into the buffer. The resultant linear regression was modeled to yield the slope values that were termed advanced glycation index (AGI) in arbitrary units. The serum levels of AGI (mean +/- SD) were higher in diabetic subjects without complications (6.0 +/- 1.6 units) compared with nondiabetic subjects (4.6 +/- 1.0 units), still higher among diabetic subjects with retinopathy (7.6 +/- 1.2 units) and highest in diabetic subjects with both retinopathy and nephropathy (8.3 +/- 2.0 units). Among diabetic subjects, AGI had a significant positive correlation with duration of diabetes (r = 0.25, P = .006), glycated hemoglobin (r = 0.27, P = .004), cholesterol (r = 0.24, P = .009), triglycerides (r = 0.23, P = .014), and serum creatinine (r = 0.30, P = .001), and a significant negative correlation with creatinine clearance (r = -0.27, P = .003). Logistic regression analysis using diabetic microangiopathy as the dependent variable showed an association with AGI even after including age, duration of diabetes, and glycated hemoglobin (P < .001) into the model. Advanced glycation index is a simple method to detect AGEs, and it correlates well with diabetes, particularly with microangiopathy.

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http://dx.doi.org/10.1016/j.metabol.2005.02.017DOI Listing
August 2005
8 Reads
6.513 Impact Factor

Is insulin signaling molecules misguided in diabetes for ubiquitin-proteasome mediated degradation?

Mol Cell Biochem 2005 Jul;275(1-2):117-25

Department of Cell and Molecular Biology, Madras Diabetes Research Foundation, 6B, Conran Smith Road, Gopalapuram, Chennai 600 086, India.

Recent mining of the human and mouse genomes, use of yeast genetics, and detailed analyses of several biochemical pathways, have resulted in the identification of many new roles for ubiquitin-proteasome mediated degradation of proteins. In the context of last year's award of Noble Prize (Chemistry) work, the ubiquitin and ubiquitin-like modifications are increasingly recognized as key regulatory events in health and disease. Although the ATP-dependent ubiquitin-proteasome system has evolved as premier cellular proteolytic machinery, dysregulation of this system by several different mechanisms leads to inappropriate degradation of specific proteins and pathological consequences. While aberrations in the ubiquitin-proteasome pathway have been implicated in certain malignancies and neurodegenerative disorders, recent studies indicate a role for this system in the pathogenesis of diabetes and its complications. Inappropriate degradation of insulin signaling molecules such as insulin receptor substrates (IRS-1 and IRS-2) has been demonstrated in experimental diabetes, mediated in part through the up-regulation of suppressors of cytokine signaling (SOCS). It appears that altered ubiquitin-proteasome system might be one of the molecular mechanisms of insulin resistance in many pathological situations. Drugs that modulate the SOCS action and/or proteasomal degradation of proteins could become novel agents for the treatment of insulin resistance and Type 2 diabetes.

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http://dx.doi.org/10.1007/s11010-005-1083-yDOI Listing
July 2005
1 Read
2.884 Impact Factor

Curcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications.

J Biosci 2003 Dec;28(6):715-21

Division of Cell and Molecular Biology, Madras Diabetes Research Foundation, 4 Conran Smith Road, Gopalapuram, Chennai 600 086, India.

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http://dx.doi.org/10.1007/bf02708432DOI Listing
December 2003
8 Reads
27 Citations
2.064 Impact Factor

Top co-authors

Vinodh Narayanan
Vinodh Narayanan

Center for Rare Childhood Disorders

11
Muthuswamy Balasubramanyam
Muthuswamy Balasubramanyam

Department of Cell and Molecular Biology

9
Keri Ramsey
Keri Ramsey

Center for Rare Childhood Disorders

8
Rangasamy Sampathkumar
Rangasamy Sampathkumar

Madras Diabetes Research Foundation and Dr. Mohans' M.V. Diabetes Specialities Centre

8
Szabolcs Szelinger
Szabolcs Szelinger

Center for Rare Childhood Disorders

7
Viswanathan Mohan
Viswanathan Mohan

Madras Diabetes Research Foundation

6
Arup Das
Arup Das

University of New Mexico School of Medicine

6
Paul G McGuire
Paul G McGuire

University of New Mexico School of Medicine

6
Ryan Richholt
Ryan Richholt

Center for Rare Childhood Disorders

5
Isabelle Schrauwen
Isabelle Schrauwen

University of Antwerp

5