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Work Phone Number:
(310) 206-6730
Work Email Address: mdc@ucla.edu
Education: Ph.D., ,
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Dr. Collins received a Ph.D. in Civil Engineering from the University of Missouri in Columbia. He then held postdoctoral fellowships at the Harvard School of Public Health and at Children's Hospital Research Foundation/University of Cincinnati. He subsequently became a faculty member in the Developmental Biology program at Cincinnati and did a sabbatical at the Freie Universitat in Berlin. He is currently a Professor in the Department of Environmental Health Sciences and an Associate Director of Student Affairs in the Interdepartmental Program in Molecular Toxicology.
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The focus of the laboratory is to determine the reasons for differential mouse strain responses to chemical agents that cause birth defects (teratogens). One of the malformations that has been induced by a wide variety of teratogens is postaxial forelimb ectrodactyly (absence of digits with the highest prevalence in the fifth digit then the fourth then the third, etc.) which occurs preferentially on the right limb as opposed to the left limb. This malformation has been produced in mice with acetazolamide, cadmium, carbon dioxide, dimethadione, diphenylhydantoin, ethanol, hyperthermia, retinoic acid (13-cis- and all-trans-) and valproic acid. These compounds include many documented human teratogens. In all cases where both the C57BL/6 and SWV mouse strains have been examined with these agents, the C57BL/6 strain is highly susceptible compared to the SWV strain. The goal of our experiments is to determine the reason for this consistent differential susceptibility. Alternatively, several teratogens have been examined in the same two strains for the ability to induce the neural tube defect exencephaly. For this malformation, the relative strain susceptibility is dependent on the specific teratogen. Thus, for some agents the C57BL/6 mouse is more susceptible and for other agents the SWV is more susceptible. Approaches that have been used to generate hypotheses regarding the cause of these strain differences include whole genome scanning followed by positional cloning, gene expression profiling, proteomic analysis, determining synexpression of limb development genes during the embryonic period following administration of the teratogen, and examining other malformations induced by the teratogens when administered at different gestational times that share the same strain susceptibility. Ongoing experiments are designed to determine the reasons for the different strain responses.
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Lee GS, Kochhar DM, Collins MD Retinoid-induced limb malformations..
Current pharmaceutical design. .
2004; 10(22):
2657-99.
Santos-Guzman J,
Arnhold T,
Nau H,
Wagner C,
Fahr SH,
Mao GE,
Caudill MA,
Wang JC,
Henning SM,
Swendseid ME,
Collins MD Antagonism of hypervitaminosis A-induced anterior neural tube closure defects with a methyl-donor deficiency in murine whole-embryo culture.
J. Nutr.
2003; 133(11):
3561-3570.
Mao GE,
Collins MD Quantitation and localization of expression of the retinoic acid receptor-beta and -gamma mRNA isoforms during neurulation in mouse embryos with or without spina bifida.
Teratology
2002; 66:
331-343.
Collins MD,
Mao GE Teratology of retinoids.
Ann. Rev. Pharmacol. Toxicol.
1999; 39:
399-430.
Lee GS, Cantor RM, Abnoosian A, Park E, Yamamoto ML, Hovland DN, Collins MD A gene(s) for all-trans-retinoic acid-induced forelimb defects mapped and confirmed to murine chromosome 11..
Genetics. .
2005; 170(1):
345-53.
Machado AF, Zimmerman EF, Hovland DN, Weiss R, Collins MD Diabetic embryopathy in C57BL/6J mice. Altered fetal sex ratio and impact of the splotch allele..
Diabetes. .
2001; 50(5):
1193-9.
Hovland DN, Cantor RM, Lee GS, Machado AF, Collins MD Identification of a murine locus conveying susceptibility to cadmium-induced forelimb malformations..
Genomics. .
2000; 63(2):
193-201.
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Work Address:
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Office
CHS
Los Angeles, CA 90095
UNITED STATES
71-297 CHS
Mailcode 177220
CA
UNITED STATES
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Work Phone Number:
(310) 206-6730
Work Email Address: mdc@ucla.edu
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