A New American University Model for Training the Future MCH Workforce Through a Translational Research Team.

OBJECTIVES: To describe the process of developing and implementing experiential learning through translational research teams that engage diverse undergraduate and graduate students. METHODS: After a college redesign, translational research teams were developed to foster multidisciplinary research and better integrate students with faculty research, community, and clinical activities. Three primary approaches were used to engage undergraduate and graduate students in the maternal and child health translational research team (MCH TrT). These included an undergraduate experiential learning course; participation in translational research team meetings and events; and mentorship activities including graduate student theses and supplementary projects. RESULTS: Since 2019, a total of 56 students have engaged with the MCH translational research team. The majority (64%) of students engaging in translational research were undergraduates. Racial and ethnic diversity was evident with 16% Latinx, 14% Black/African American, 12% Asian, 10% two or more races, and 4% Native American or Native Hawaiian. A large proportion (42%) of students indicated that they were first-generation college students, while 24% indicated they had a disability. Five themes emerged from student feedback about their involvement in the experiential learning course: the value of translational research, development of research skills, collaboration, practice development, and value for community partners. CONCLUSIONS FOR PRACTICE: Through an MCH translational research team, we have established a pathway to enhance diversity among the MCH workforce which will increase recruitment and retention of underrepresented groups, and ultimately improve MCH research and practice.

Insulin-induced GLUT4 translocation involves protein kinase C-lambda-mediated functional coupling between Rab4 and the motor protein kinesin.

Insulin stimulates glucose transport by promoting translocation of GLUT4 proteins from the perinuclear compartment to the cell surface. It has been previously suggested that the microtubule-associated motor protein kinesin, which transports cargo toward the plus end of microtubules, plays a role in translocating GLUT4 vesicles to the cell surface. In this study, we investigated the role of Rab4, a small GTPase-binding protein, and the motor protein KIF3 (kinesin II in mice) in insulin-induced GLUT4 exocytosis in 3T3-L1 adipocytes. Photoaffinity labeling of Rab4 with [gamma-(32)P]GTP-azidoanilide showed that insulin stimulated Rab4 GTP loading and that this insulin effect was inhibited by pretreatment with the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor LY294002 or expression of dominant-negative protein kinase C-lambda (PKC-lambda). Consistent with previous reports, expression of dominant-negative Rab4 (N121I) decreased insulin-induced GLUT4 translocation by 45%. Microinjection of an anti-KIF3 antibody into 3T3-L1 adipocytes decreased insulin-induced GLUT4 exocytosis by 65% but had no effect on endocytosis. Coimmunoprecipitation experiments showed that Rab4, but not Rab5, physically associated with KIF3, and this was confirmed by showing in vitro association using glutathione S-transferase-Rab4. A microtubule capture assay demonstrated that insulin stimulation increased the activity for the binding of KIF3 to microtubules and that this activation was inhibited by pretreatment with the PI3-kinase inhibitor LY294002 or expression of dominant-negative PKC-lambda. Taken together, these data indicate that (i) insulin signaling stimulates Rab4 activity, the association of Rab4 with kinesin, and the interaction of KIF3 with microtubules and (ii) this process is mediated by insulin-induced PI3-kinase-dependent PKC-lambda activation and participates in GLUT4 exocytosis in 3T3-L1 adipocytes.