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Chatterjee Bhowmick, D.

Publications and source records attributed to Chatterjee Bhowmick, D..

2 recordsLinked to original sources

Loss of Exocytosis Protein DOC2B is an Early Event in Type 1 Diabetes Development

Abstract: Type 1 diabetes (T1D) affects millions worldwide, yet few non-invasive biomarkers detect immune-mediated {beta}-cell dysfunction during the presymptomatic phase, a critical window for therapeutic intervention. Previously, we identified reduced double C2-like domain containing beta protein (DOC2B) levels in circulating platelets as a marker of reduced {beta}-cell function in early-onset T1D cohorts and nonobese diabetic (NOD) mice. Here, we assessed whether plasma DOC2B could serve as a sensitive early biomarker of T1D progression risk in the autoantibody-positive pediatric cohort (progressors vs non-progressors) from the longitudinal Diabetes Evaluation in Washington (DEW-IT) study; T1D patients and non-diabetic cohorts from the DEW-IT study served as controls. At pre-onset, progressors showed a decline in DOC2B that preceded measurable changes in random C-peptide and HbA1c levels, while non-progressors maintained stable levels. These observations were further supported by our analysis in prediabetic NOD mice. Comparisons of plasma levels pre- and post-clinical islet transplantation in long-standing T1D patients highlights its potential utility as a reporter of {beta}-cell functional mass. Together, these findings suggest that DOC2B decline may precede C-peptide decline in early presymptomatic T1D progression. This work could have significant future implications for clinical trial stratification and assessing response outcomes to disease-modifying or cell replacement therapies.

physiology↗

DOC2b enrichment mitigates proinflammatory cytokine-induced CXCL10 expression by attenuating IKKβ and STAT-1 signaling in human islets

IntroductionType 1 diabetic human islet {beta}-cells are deficient in double C 2 like domain beta (DOC2b) protein. Further, DOC2b protects against cytokine-induced pancreatic islet {beta}-cell stress and apoptosis. However, the mechanisms underpinning the protective effects of DOC2b remain unknown. MethodsBiochemical studies, qPCR, proteomics, and immuno-confocal microscopy were conducted to determine the underlying protective mechanisms of DOC2b in {beta}-cells. DOC2b- enriched or-depleted primary islets (human and mouse) and {beta}-cell lines challenged with or without proinflammatory cytokines, global DOC2b heterozygous knockout mice subjected to multiple-low-dose-streptozotocin (MLD-STZ), were used for these studies. ResultsA significant elevation of stress-induced CXCL10 mRNA was observed in DOC2b- depleted {beta}-cells and primary mouse islets. Further, DOC2b enrichment markedly attenuated cytokine-induced CXCL10 levels in primary non-diabetic human islets and {beta}-cells. DOC2b enrichment also reduced total-NF-{kappa}B p65 protein levels in human islets challenged with T1D mimicking proinflammatory cytokines. IKK{beta}, NF-{kappa}B p65, and STAT-1 are capable of associating with DOC2b in cytokine-challenged {beta}-cells. DOC2b enrichment in cytokine-stressed human islets and {beta}-cells corresponded with a significant reduction in activated and total IKK{beta} protein levels. Total I{kappa}B{beta} protein was increased in DOC2b-enriched human islets subjected to acute cytokine challenge. Cytokine-induced activated and total STAT-1 protein and mRNA levels were markedly reduced in DOC2b-enriched human islets. Intriguingly, DOC2b also prevents ER-stress-IKK{beta} and STAT-1 crosstalk in the rat INS1-832/13 {beta}-cell line. ConclusionThe mechanisms underpinning the protective effects of DOC2b involve attenuation of IKK{beta}-NF-{kappa}B p65 and STAT-1 signaling, and reduced CXCL10 expression. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=179 HEIGHT=200 SRC="FIGDIR/small/629540v1_ufig1.gif" ALT="Figure 1"> View larger version (33K): org.highwire.dtl.DTLVardef@1b9d0acorg.highwire.dtl.DTLVardef@32db73org.highwire.dtl.DTLVardef@e5645aorg.highwire.dtl.DTLVardef@1f7619_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗