Publications by authors named "B D Garfinkel"

Aims: One unaddressed aspect of healing after myocardial infarction (MI) is how non-myocyte cells that survived the ischemic injury, keep withstanding additional cellular damage by stress forms typically arising during the post-infarction inflammation. Here we aimed to determine if cell survival is conferred by expression of a mitochondrial protein novel to the cardiac proteome, known as steroidogenic acute regulatory protein, (StAR/STARD1). Further studies aimed to unravel the regulation and role of the non-steroidogenic cardiac StAR after MI.

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Alzheimer's disease (AD) involves changes in both lipid and RNA metabolism, but it remained unknown if these differences associate with AD's cognition and/or post-mortem neuropathology indices. Here, we report RNA-sequencing evidence of inter-related associations between lipid processing, cognition level, and AD neuropathology. In two unrelated cohorts, we identified pathway-enriched facilitation of lipid processing and alternative splicing genes, including the neuronal-enriched NOVA1 and hnRNPA1.

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A new mechanism linking ER dysfunction to metabolic inflammation is discovered in a recent study by Shan et al. (2017), which demonstrated ER stress-induced rewiring of adipose tissue macrophage polarization by IRE1α activation, leading to impaired systemic glucose homeostasis.

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Alzheimer's disease is a devastating neurodegenerative disorder affecting a significant portion of the world's rapidly growing aging population. In spite of its prevalence, the etiology of the disease is still poorly understood, and effective therapy is all but unavailable. Over the past decade, noncoding RNA, including microRNA (miRNA), has emerged as a major class of regulatory molecules involved in virtually all physiological and disease states.

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Maternal care is an indispensable behavioral component necessary for survival and reproductive success in mammals, and postpartum maternal behavior is mediated by an incompletely understood complex interplay of signals including effects of epigenetic regulation. We approached this issue using our recently established mice with targeted deletion of heterochromatin protein 1 binding protein 3 (HP1BP3), which we found to be a novel epigenetic repressor with critical roles in postnatal growth. Here, we report a dramatic reduction in the survival of pups born to Hp1bp3(-/-) deficient mouse dams, which could be rescued by co-fostering with wild-type dams.

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