Stanley Andrisse, MBA, PhD
Baltimore, Maryland, United States
8K followers
500+ connections
About
Department of Physiology and Biophysics
I am a tenure-track Assistant Professor…
Activity
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*Howard University Public Event* Join us as we commemorate the 70th anniversary of the Brown v. Board of Education decision which declared segregated…
*Howard University Public Event* Join us as we commemorate the 70th anniversary of the Brown v. Board of Education decision which declared segregated…
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I have some exciting news to share! From Prison Cells to PhD (P2P) is thrilled to announce the upcoming graduation of our Prison to Professionals…
I have some exciting news to share! From Prison Cells to PhD (P2P) is thrilled to announce the upcoming graduation of our Prison to Professionals…
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I would like to take a moment to spotlight one of From Prison Cells to PhD's (P2P) Staff Members. Judith Negron is an inspiring member of our staff…
I would like to take a moment to spotlight one of From Prison Cells to PhD's (P2P) Staff Members. Judith Negron is an inspiring member of our staff…
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Experience
Education
Volunteer Experience
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Youth Mentor
Youth Mentor
Big Brothers Big Sisters of the Greater Chesapeake
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STEM Facilitator
STEM Achievement in Baltimore Elementary Schools (SABES)
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Mentor, Aim to B'More
Mentor, Aim to B'More
Office of the State's Attorney for Baltimore City
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Member Board of Directors, AGPEP
Member Board of Directors, AGPEP
Goucher College
Publications
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Androgen Receptor in the Ovary Theca Cells Plays a Critical Role in Androgen-Induced Reproductive Dysfunction
Endocrinology
Androgen and its receptor (AR) plays a critical role in reproductive function, under both physiological and pathophysiological conditions. Female AR global knockout mice are sub-fertile due to both neuroendocrine and ovarian defects. Female offspring from prenatally androgenized heterozygous AR pregnant mice showed rescued estrous cyclicity and fertility. Ar is expressed in granulosa cells, theca interstitial cells, and oocytes in the ovary. We created mice with theca-specific deletion of Ar…
Androgen and its receptor (AR) plays a critical role in reproductive function, under both physiological and pathophysiological conditions. Female AR global knockout mice are sub-fertile due to both neuroendocrine and ovarian defects. Female offspring from prenatally androgenized heterozygous AR pregnant mice showed rescued estrous cyclicity and fertility. Ar is expressed in granulosa cells, theca interstitial cells, and oocytes in the ovary. We created mice with theca-specific deletion of Ar (ThARKO) by crossing Cyp17-iCre mice that express Cre recombinase under Cyp17 promoter with Arfl/fl mice. ThARKO mice exhibited no significant differences in pubertal onset or fertility compared with control littermates, and neither estrogen and testosterone levels were different between these groups. Therefore, Ar expression in theca cells likely does not influence fertility nor androgen levels in female mice. We then tested the role of AR in theca cells under hyperandrogenemic condition. After treatment with a pathophysiological level of dihydrotestosterone (DHT), control mice (Con-DHT) showed acyclicity and infertility. However, estrous cycles and fertility were altered to a significantly less degree in ThARKO-DHT mice than in Con-DHT mice. Three months after DHT treatment, mRNA levels of Lhcgr (luteinizing hormone receptor) and, Timp1 (tissue inhibitor of metalloproteinase 1, and inhibitor of matrix metalloproteinase (MMP)) were significantly lower in Con-DHT ovary compared to Con-no DHT ovary; whereas mRNA levels of Fshr (follicle stimulating hormone receptor) were significantly higher. Timp1 gene expression was comparable in the ThARKO-DHT ovary and the Con-no DHT ovary. We speculate that the preserved level of Timp1 in ThARKO-DHT mice contributes to retained reproductive function.
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Role of GLUT1 in regulation of reactive oxygen species.
Redox Biology
In skeletal muscle cells, GLUT1 is responsible for a large portion of basal uptake of glucose and dehydroascorbic acid, both of which play roles in antioxidant defense. We hypothesized that conditions that would decrease GLUT1-mediated transport would cause increased reactive oxygen species (ROS) levels in L6 myoblasts, while conditions that would increase GLUT1-mediated transport would result in decreased ROS levels. We found that the GLUT1 inhibitors fasentin and phloretin increased the ROS…
In skeletal muscle cells, GLUT1 is responsible for a large portion of basal uptake of glucose and dehydroascorbic acid, both of which play roles in antioxidant defense. We hypothesized that conditions that would decrease GLUT1-mediated transport would cause increased reactive oxygen species (ROS) levels in L6 myoblasts, while conditions that would increase GLUT1-mediated transport would result in decreased ROS levels. We found that the GLUT1 inhibitors fasentin and phloretin increased the ROS levels induced by antimycin A and the superoxide generator pyrogallol. However, indinavir, which inhibits GLUT4 but not GLUT1, had no effect on ROS levels. Ataxia telangiectasia mutated (ATM) inhibitors and activators, previously shown to inhibit and augment GLUT1-mediated transport, increased and decreased ROS levels, respectively. Mutation of an ATM target site on GLUT1 (GLUT1-S490A) increased ROS levels and prevented the ROS-lowering effect of the ATM activator doxorubicin. In contrast, expression of GLUT1-S490D lowered ROS levels during challenge with pyrogallol, prevented an increase in ROS when ATM was inhibited, and prevented the pyrogallol-induced decrease in insulin signaling and insulin-stimulated glucose transport. Taken together, the data suggest that GLUT1 plays a role in regulation of ROS and could contribute to maintenance of insulin action in the presence of ROS.
Other authorsSee publication -
ATM and GLUT1-S490 phosphorylation regulate GLUT1 mediated transport in skeletal muscle.
PLoS One
OBJECTIVE: The glucose and dehydroascorbic acid (DHA) transporter GLUT1 contains a phosphorylation site, S490, for ataxia telangiectasia mutated (ATM). The objective of this study was to determine whether ATM and GLUT1-S490 regulate GLUT1.
RESEARCH DESIGN AND METHODS: L6 myoblasts and mouse skeletal muscles were used to study the effects of ATM inhibition, ATM activation, and S490 mutation on GLUT1 localization, trafficking, and transport activity.
RESULTS:In myoblasts, inhibition…OBJECTIVE: The glucose and dehydroascorbic acid (DHA) transporter GLUT1 contains a phosphorylation site, S490, for ataxia telangiectasia mutated (ATM). The objective of this study was to determine whether ATM and GLUT1-S490 regulate GLUT1.
RESEARCH DESIGN AND METHODS: L6 myoblasts and mouse skeletal muscles were used to study the effects of ATM inhibition, ATM activation, and S490 mutation on GLUT1 localization, trafficking, and transport activity.
RESULTS:In myoblasts, inhibition of ATM significantly diminished cell surface GLUT1, glucose and DHA transport, GLUT1 externalization, and association of GLUT1 with Gα-interacting protein-interacting protein, C-terminus (GIPC1), which has been implicated in recycling of endosomal proteins. In contrast, ATM activation by doxorubicin (DXR) increased DHA transport, cell surface GLUT1, and the GLUT1/GIPC1 association. S490A mutation decreased glucose and DHA transport, cell surface GLUT1, and interaction of GLUT1 with GIPC1, while S490D mutation increased transport, cell surface GLUT1, and the GLUT1/GIPC1 interaction. ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus. In contrast, DXR increased DHA transport in EDL.
CONCLUSIONS: These results provide evidence that ATM and GLUT1-S490 promote cell surface GLUT1 and GLUT1-mediated transport in skeletal muscle associated with upregulation of the GLUT1/GIPC1 interaction.Other authorsSee publication -
Impaired insulin-stimulated glucose transport in ATM-deficient mouse skeletal muscle.
Applied Physiology, Nutrition, and Metabolism
There are reports that ataxia telangiectasia mutated (ATM) plays a role in insulin-stimulated Akt phosphorylation, although this is not the case in some cell types. Because Akt plays a key role in insulin signaling, which leads to glucose transport in skeletal muscle, the predominant tissue in insulin-stimulated glucose disposal, we examined whether insulin-stimulated Akt phosphorylation and (or) glucose transport would be decreased in skeletal muscle of mice lacking functional ATM, compared…
There are reports that ataxia telangiectasia mutated (ATM) plays a role in insulin-stimulated Akt phosphorylation, although this is not the case in some cell types. Because Akt plays a key role in insulin signaling, which leads to glucose transport in skeletal muscle, the predominant tissue in insulin-stimulated glucose disposal, we examined whether insulin-stimulated Akt phosphorylation and (or) glucose transport would be decreased in skeletal muscle of mice lacking functional ATM, compared with muscle from wild-type mice. We found that in vitro insulin-stimulated Akt phosphorylation was normal in soleus muscle from mice with 1 nonfunctional allele of ATM (ATM+/-) and from mice with 2 nonfunctional alleles (ATM-/-). However, insulin did not stimulate glucose transport or the phosphorylation of AS160 in ATM-/- soleus. ATM protein level was markedly higher in wild-type extensor digitorum longus (EDL) than in wild-type soleus. In EDL from ATM-/- mice, insulin did not stimulate glucose transport. However, in contrast to findings for soleus, insulin-stimulated Akt phosphorylation was blunted in ATM-/- EDL, concomitant with a tendency for insulin-stimulated phosphatidylinositol 3-kinase activity to be decreased. Together, the findings suggest that ATM plays a role in insulin-stimulated glucose transport at the level of AS160 in muscle comprised of slow and fast oxidative-glycolytic fibers (soleus) and at the level of Akt in muscle containing fast glycolytic fibers (EDL).
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AMP-activated protein kinase
Encyclopedia of Exercise Medicine in Health and Disease
Honors & Awards
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INCLUDES Alliance - STEM-OPS
National Science Foundation
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Philanthropic 5
United Way
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Loan Repayment Program
National Institutes of Health, NICHD
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Provost's Postdoctoral Diversity Fellowship
Johns Hopkins University Office of the Provost
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Porter Physiology Development Fellowship Grant
American Physiological Society
Languages
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French
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Haitian Creole
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Organizations
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Endocrine Society
Leadership Development Task Force
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American Physiological Society
Porter Fellow
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Signing this e-card is easy and free. Be a cheer leader for those on their scholarly journey with the Prison to Professionals program. See post to…
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