Professional Education

  • Doctor of Philosophy, Unlisted School (2023)
  • Bachelor of Science, North South University (2018)
  • Doctor of Philosophy, University of Arkansas for Medical Sciences (2023)

Stanford Advisors

All Publications

  • Musashi Exerts Control of Gonadotrope Target mRNA Translation During the Mouse Estrous Cycle. Endocrinology Moreira, A. R., Lim, J., Urbaniak, A., Banik, J., Bronson, K., Lagasse, A., Hardy, L., Haney, A., Allensworth, M., Miles, T. K., Gies, A., Byrum, S. D., Wilczynska, A., Boehm, U., Kharas, M., Lengner, C., MacNicol, M. C., Childs, G. V., MacNicol, A. M., Odle, A. K. 2023; 164 (9)


    The anterior pituitary controls key biological processes, including growth, metabolism, reproduction, and stress responses through distinct cell types that each secrete specific hormones. The anterior pituitary cells show a remarkable level of cell type plasticity that mediates the shifts in hormone-producing cell populations that are required to meet organismal needs. The molecular mechanisms underlying pituitary cell plasticity are not well understood. Recent work has implicated the pituitary stem cell populations and specifically, the mRNA binding proteins of the Musashi family in control of pituitary cell type identity. In this study we have identified the target mRNAs that mediate Musashi function in the adult mouse pituitary and demonstrate the requirement for Musashi function in vivo. Using Musashi RNA immunoprecipitation, we identify a cohort of 1184 mRNAs that show specific Musashi binding. Identified Musashi targets include the Gnrhr mRNA, which encodes the gonadotropin-releasing hormone receptor (GnRHR), and the Fshb mRNA, encoding follicle-stimulating hormone (FSH). Reporter assays reveal that Musashi functions to exert repression of translation of the Fshb mRNA, in addition to the previously observed repression of the Gnrhr mRNA. Importantly, mice engineered to lack Musashi in gonadotropes demonstrate a failure to repress translation of the endogenous Gnrhr and Fshb mRNAs during the estrous cycle and display a significant heterogeneity in litter sizes. The range of identified target mRNAs suggests that, in addition to these key gonadotrope proteins, Musashi may exert broad regulatory control over the pituitary proteome in a cell type-specific manner.

    View details for DOI 10.1210/endocr/bqad113

    View details for PubMedID 37477898

    View details for PubMedCentralID PMC10402870

  • Control of the Anterior Pituitary Cell Lineage Regulator POU1F1 by the Stem Cell Determinant Musashi. Endocrinology Allensworth-James, M., Banik, J., Odle, A., Hardy, L., Lagasse, A., Moreira, A. R., Bird, J., Thomas, C. L., Avaritt, N., Kharas, M. G., Lengner, C. J., Byrum, S. D., MacNicol, M. C., Childs, G. V., MacNicol, A. M. 2021; 162 (3)


    The adipokine leptin regulates energy homeostasis through ubiquitously expressed leptin receptors. Leptin has a number of major signaling targets in the brain, including cells of the anterior pituitary (AP). We have previously reported that mice lacking leptin receptors in AP somatotropes display growth hormone (GH) deficiency, metabolic dysfunction, and adult-onset obesity. Among other targets, leptin signaling promotes increased levels of the pituitary transcription factor POU1F1, which in turn regulates the specification of somatotrope, lactotrope, and thyrotrope cell lineages within the AP. Leptin's mechanism of action on somatotropes is sex dependent, with females demonstrating posttranscriptional control of Pou1f1 messenger RNA (mRNA) translation. Here, we report that the stem cell marker and mRNA translational control protein, Musashi1, exerts repression of the Pou1f1 mRNA. In female somatotropes, Msi1 mRNA and protein levels are increased in the mouse model that lacks leptin signaling (Gh-CRE Lepr-null), coincident with lack of POU1f1 protein, despite normal levels of Pou1f1 mRNA. Single-cell RNA sequencing of pituitary cells from control female animals indicates that both Msi1 and Pou1f1 mRNAs are expressed in Gh-expressing somatotropes, and immunocytochemistry confirms that Musashi1 protein is present in the somatotrope cell population. We demonstrate that Musashi interacts directly with the Pou1f1 mRNA 3' untranslated region and exerts translational repression of a Pou1f1 mRNA translation reporter in a leptin-sensitive manner. Musashi immunoprecipitation from whole pituitary reveals coassociated Pou1f1 mRNA. These findings suggest a mechanism in which leptin stimulation is required to reverse Musashi-mediated Pou1f1 mRNA translational control to coordinate AP somatotrope function with metabolic status.

    View details for DOI 10.1210/endocr/bqaa245

    View details for PubMedID 33373440

    View details for PubMedCentralID PMC7814296

  • Activation of GPR35 protects against cerebral ischemia by recruiting monocyte-derived macrophages. Scientific reports Sharmin, O., Abir, A. H., Potol, A., Alam, M., Banik, J., Rahman, A. F., Tarannum, N., Wadud, R., Habib, Z. F., Rahman, M. 2020; 10 (1): 9400


    Pamoic acid is a potent ligand for G protein Coupled Receptor 35 (GPR35) and exhibits antinociceptive property. GPR35 activation leads to increased energy utilization and the expression of anti-inflammatory genes. However, its role in brain disorders, especially in stroke, remains unexplored. Here we show in a mouse model of stroke that GPR35 activation by pamoic acid is neuroprotective. Pharmacological inhibition of GPR35 reveals that pamoic acid reduces infarcts size in a GPR35 dependent manner. The flowcytometric analysis shows the expression of GPR35 on the infiltrating monocytes/macrophages and neutrophils in the ischemic brain. Pamoic acid treatment results in a preferential increment of noninflammatory Ly-6CLo monocytes/macrophages in the ischemic brain along with the reduced neutrophil counts. The neuroprotective effect of GPR35 activation depends on protein kinase B (Akt) and p38 MAPK. Together we conclude that GPR35 activation by pamoic acid reprograms Ly-6CLo monocytes/macrophages to relay a neuroprotective signal into the ischemic brain.

    View details for DOI 10.1038/s41598-020-66417-8

    View details for PubMedID 32523084

    View details for PubMedCentralID PMC7287103