Santosh K. Katiyar, Ph.D.

SantoshKatiyar2009

University of Alabama at Birmingham
VH 557
1530 3RD AVE S
BIRMINGHAM AL 35294-0019

Office: (205)975-2608
skatiyar@uab.edu

 

 

 

Education

B.S.               Chemistry, Zoology and Botany, 1971
M.S.               Chemistry, Kanpur University, Kanpur, India, 1975
Ph. D.            Chemistry, Bundelkhand University, Jhansi, India, 1979
Fellowship   Post-doctoral Fellow, Biochemistry Department, Allahabad
                        University,Allahabad, India, 1979 - 1982

 

 Academic Appointments

Scientist

 

Department of Food Technology, Regional Research Laboratory, Jammu, India 1991

Senior Research Associate                                                 

 

Case Western Reserve University, Cleveland, OH, 1991-2000

Tenured Professor

 

Department of Dermatology, School of Medicine, UAB

Senior Scientist

 

Comprehensive Cancer Center, UAB

Professor

 

Department of Environmental Health Sciences, School of Public Health, UAB

Scientist

 

Center for Aging, UAB

Research Center Scientist

  

Veterans Administration Medical Center, Birmingham, AL

 


RESEARCH INTEREST IN CUTANEOUS BIOLOGY

 Dr. Katiyar has been working for the last 13 years on different aspects of cutaneous biology, such as immunology, photobiology, photocarcinogenesis and photoaging, as detailed below:

 Causes, mechanism and preventive approaches of skin carcinogenesis

 Dr. Katiyar's interest is to study and/or determine the causes, mechanisms and preventiom of chemical and solar ultraviolet (UV) radiation induced skin carcinogenesis (photocarcinogenesis). It is well documented that chronic exposure of solar UV radiation to human skin is primarily responsible for approximately 1.3 million new cases of squamous and basal cell carcinoma every year in the USA, thus making it the most prevalent environmental carcinogen known for humans. UV radiation is a potent producer of reactive oxygen species and can act as a tumor initiator, tumor promoter and complete carcinogen as well. Dr. Katiyar is trying to develop newer and effective chemopreventive agents, particularly dietary botanicals that can prevent the risk of UV carcinogenesis in humans. To develop newer and more effective chemopreventive agents, we use in vivo animal and human model systems and in vitro cell culture systems.

In particular, he is evaluating the chemopreventive efficacy of polyphenols isolated from green tea, milk thistle and grape seeds. Dr. Katiyar has shown that these polyphenols have anti-inflammatory and anti-oxidant properties. Because of these characteristics, polyphenols have been shown to inhibit, reverse or slow down the risk of UV-induced skin carcinogenesis. To determine the mechanism of action of these naturally occurring polyphemols or dietary botanicals, he is particularly emphasizing the anti-oxidant mechanism and modulation in immunoregulatory pathways responsible for inhibition of UV-induced adverse biological effects.

 Causes, mechanism and preventive approaches of cutaneous photoaging

 As in other organ systems, aging in the skin results in progressive dysfunction and diminution of the radiation reserve capacity under stress, rendering the skin more susceptible to injury and diseases. Clinical conditions associated with age-dependent dysfunction include increased ease of wounding, poor wound healing, skin cancer and infectious disease susceptibility, autoimmune reactivity to skin and drugs. The progressive susceptibility to these conditions with age is due to a combination of aging processes attributable to both chronologic (intrinsic) aging, and photoaging (extrinsic damage from the environment, mainly repeated solar light exposure). Clinically the photoaging component of skin aging accounts for the development in sun-exposed areas of wrinkling, mottled hyperpigmentation and depigmentation, coarsening of the skin, roughness, poor elastic recoil, and bruisability. These conditions adversely affect self-esteem and psychosocial well being. By contrast, intervention to reduce the stigmata of photoaging can result in improved quality of life and functionality in the elderly. Dr. Katiyar also considers that accelerated photoaging of the skin is also due to impaired oxidative defense system.

 Keeping these factors under consideration, Dr. Katiyar is developing new and effective chemopreventive agents, particularly from dietary sources, which can inhibit the process of skin aging and photoaging. For this purpose, he is working on various polyphenols obtained from green tea and grape seeds and using in vitro and in vivo model systems. He determined that topical application of polyphenols from green tea on animal skin protects from UV-induced adverse biological effects associated with the photoaging of the skin.


Publications: From total more than 170 publications and 15 Book Chapters

 Meeran SM, Akhtar S and Katiyar SK: Inhibition of UVB-induced skin tumor development by drinking green tea polyphenols is mediated through DNA repair and subsequent inhibition of inflammation. J. Invest. Dermatol., 129: 1258-1270, 2009.

Vaid M, Sharma SD, Katiyar SK: Honokiol, a phytochemical from the Magnolia plant, inhibits photocarcinogenesis by targeting UVB-induced inflammatory mediators and cell cycle regulators: Development of topical formulation. Carcinogenesis, 31: 2004-2011, 2010. 

Nandakumar V, Vaid M, Tollefsbol TO, Katiyar SK: Aberrant DNA hypermethylation patterns lead to transcriptional silencing of tumor suppressor genes in UVB-exposed skin and UVB-induced skin tumors of mice. Carcinogenesis, 32: 597-604, 2011.

Vaid M, Singh T, Li A, Katiyar N, Sharma S, Elmets CA, Xu H and Katiyar SK: Proanthocyanidins inhibit UV-induced immunosuppression through IL-12-dependent stimulation of CD8+ effector T cells and inactivation of CD4+ T cells. Cancer Prev. Res., 4: 238-247, 2011.

Vaid M, Singh T, Prasad R, Elmets CA, Xu H and Katiyar SK: Bioactive grape proanthocyanidins enhance immune reactivity in UV-irradiated skin through functional activation of dendritic cells in mice. Cancer Prev. Res., 6: 242-252, 2013.

 Mantena SK and Katiyar SK: Grape seed proanthocyanidins inhibit UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling in human epidermal keratinocytes. Free Rad. Biol. Med., 40: 1603-1614, 2006.

Meeran SM, Mantena SK, Elmets CA and Katiyar SK: (-)-Epigallocatechin-3-gallate prevents photocarcinogenesis in mice through interleukin-12-dependent DNA repair. Cancer Res., 66:5512-5520, 2006.

Yusuf N, Nasti TH, Katiyar SK, Jacobs MK, Seibert MD, Ginsburg AC, Timares L, Xu H and Elmets CA: Antagonistic roles of CD4+ and CD8+ T-cells in 7,12-dimethylbenz(a)anthracene cutaneous carcinogenesis. Cancer Res., 68 (10): 3924-3930, 2008.

Timares L, Katiyar SK and Elmets CA: DNA damage, apoptosis and Langerhans cells- activators of UV-induced immune tolerance. Photochem. Photobiol., 84: 422-436, 2008.

Katiyar SK, Vaid M, van Steeg H and Meeran SM: Green tea polyphenols prevent UV-induced immunosuppression by rapid repair of DNA damage and enhancement of nucleotide excision repair genes. Cancer Prev. Res., 3: 179-189, 2010.

Nandakumar V, Vaid M, Katiyar SK: (-)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. Carcinogenesis, 32: 537-544, 2011.

Vaid M, Prasad R, Singh T, Jones V, Katiyar SK: Grape seed proanthocyanidins reactivate silenced tumor suppressor genes in human skin cancer cells by targeting epigenetic regulators. Toxicol Appl Pharmacol, 263: 122-130, 2012.

Katiyar SK, Singh T, Prasad R, Sun Q, Vaid M: Epigenetic alterations in ultraviolet radiation-induced skin carcinogenesis: Interaction of bioactive dietary components on epigenetic targets. Photochem. Photobiol., 88: 1066-1074, 2012.

Singh T, Prasad R and Katiyar SK: Inhibition of class I histone deacetylases in non-small cell lung cancer by honokiol leads to suppression of cancer cell growth and induction of cell death in vitro and in vivo. Epigenetics, 8:54-65, 2013.

 GRANTS SUPPORT

National Institute of Health/ National Cancer Institute
Project entitled: "Prevention of UV-carcinogenesis through DNA repair-dependent immunomodulation
Principal Investigator
Project Period: 07/01/2010-12/31/2014

National Institute of Health/ National Cancer Institute
Project entitled: "Proanthocyanidins, novel bioactive components for prevention of melanoma invasion"
Prinicpal Investigator
Project Period:  01/01/2013-12/31/2014

 
VA Merit Review Award, Veterans Administration
Project entitled: "Prevention of photocarcinogenesis by dietary immunomodulation"
Principal Investigator
Period: 04/01/2008-03/31/2016