A5005096737- Eicosanoids and Hypertension Pharmacology
- Adipose Tissue and Metabolism
- Sleep and Wakefulness Research
- Autophagy in Disease and Therapy
- Regulation of Appetite and Obesity
- Parkinson's Disease Mechanisms and Treatments
- Biochemical Acid Research Studies
- Peroxisome Proliferator-Activated Receptors
- Alzheimer's disease research and treatments
- Hormonal Regulation and Hypertension
- Cellular transport and secretion
- RNA Interference and Gene Delivery
- Receptor Mechanisms and Signaling
- Lysosomal Storage Disorders Research
- Metabolism and Genetic Disorders
- Calcium signaling and nucleotide metabolism
- Renin-Angiotensin System Studies
- Pancreatic function and diabetes
- Plant responses to water stress
- Pharmacogenetics and Drug Metabolism
- Alcohol Consumption and Health Effects
- Nitric Oxide and Endothelin Effects
- Biochemical effects in animals
- Diabetes Management and Research
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
Rutgers New Jersey Medical School
2019-2024
Rutgers, The State University of New Jersey
2019-2024
Nathan Kline Institute for Psychiatric Research
2018
Cornell University
2013-2014
Medical College of Wisconsin
2011-2013
Autophagy-lysosome pathway (ALP) disruption is considered pathogenic in multiple neurodegenerative diseases; however, current methods are inadequate to investigate macroautophagy/autophagy flux brain vivo and its therapeutic modulation. Here, we describe a novel autophagy reporter mouse (TRGL6) stably expressing dual-fluorescence-tagged LC3 (tfLC3, mRFP-eGFP-LC3) by transgenesis selectively neurons. The tfLC3 probe distributes widely the central nervous system, including spinal cord....
Amyloid-β (Aβ) has long been implicated as a causative protein in Alzheimer's disease. Cellular Aβ accumulation is toxic and causes mitochondrial dysfunction, which precedes clinical symptoms of disease pathology. In the present study, we explored possible use epoxyeicosatrienoic acids (EETs), epoxide metabolites arachidonic acid, therapeutic target against Aβ-induced impairment using cultured neonatal hippocampal astrocytes. Inhibition endogenous EET production by selective epoxygenase...
Regulation of blood pressure by angiotensin II (ANG II) is a process that involves the reactive oxygen species (ROS) and calcium. We have shown ANG-II type 1 receptor (AT1R) prostaglandin E2 (PGE2) receptors (EP1R) are required in subfornical organ (SFO) for ROS-mediated hypertension induced slow-pressor infusion. However, signaling pathway associated with this remains unclear. sought to determine mechanisms underlying ANG II-induced ROS calcium influx mouse SFO cells. Ultrastructural...
Perifornical hypothalamus (PFH) orexin glucose-inhibited (GI) neurons that facilitate arousal have been implicated in hypoglycemia awareness. Mice lacking exhibit narcolepsy, and mediates the effect of antinarcolepsy drug modafinil. Thus, awareness may require a certain level for sympathetic symptoms (e.g., tremors, anxiety). Recurrent (RH) causes unawareness. We hypothesize RH impairs glucose sensitivity PFH GI modafinil normalizes these restores after RH. Using patch-clamp recording, we...
Pathogenic activating point mutations in the LRRK2 kinase cause autosomal-dominant familial Parkinsońs disease (PD). In cultured cells, mutant causes a deficit de novo cilia formation and also impairs ciliary stability. brain, previous studies have shown that PD patients due to G2019S-LRRK2 mutation as well middle-aged knockin mice, striatal cholinergic interneurons show primary cilia. Here, we loss mice is not limited but common neurons across distinct brain nuclei. The lack of forebrain...
Glucose-inhibited (GI) neurons of the ventromedial hypothalamus (VMH) depend on neuronal nitric oxide synthase (nNOS) and AMP-activated protein kinase (AMPK) for activation in low glucose. The Lopez laboratory has shown that effects estrogen brown fat thermogenesis white browning require inhibition VMH AMPK. This effect was mediated by downstream lateral (LH) orexin (1,2). We previously showed inhibits GI glucose inhibiting AMPK (3). Thus, we hypothesized AMPK- nNOS-dependent project to...
Abstract Pathogenic activating point mutations in the LRRK2 kinase cause autosomal-dominant familial Parkinsońs disease (PD). In cultured cells, mutant causes a deficit de novo cilia formation and also impairs ciliary stability. brain, previous studies have shown that PD patients due to G2019S-LRRK2 mutation as well middle-aged knockin mice, striatal cholinergic interneurons show primary cilia. Here, we loss mice is not limited but common neurons across distinct brain nuclei. The lack of...
Pathogenic activating point mutations in the LRRK2 kinase cause autosomal-dominant familial Parkinsońs disease (PD). In cultured cells, mutant causes a deficit de novo cilia formation and also impairs ciliary stability. brain, previous studies have shown that PD patients due to G2019S-LRRK2 mutation as well middle-aged knockin mice, striatal cholinergic interneurons show primary cilia. Here, we loss mice is not limited but common neurons across distinct brain nuclei. The lack of forebrain...
ER stress and mROS are identified as key mediators of Ang-II-induced neurogenic hypertension. Although mitochondria linked both structurally functionally, the interplay between these two organelles in neural cells subfornical organ (SFO), a forebrain region Ang-II hypertension, is unknown. Previously we reported that causes mitochondrial fragmentation murine SFO neurons. Here tested hypothesis Ang II-induced dysfunction mediated by disruption MAM. Neuro-2A were incubated with (300 nM, 24 h)...
The SFO plays a critical role in the development of hypertension response to elevated levels circulating Ang II. Recent evidence suggests that peripheral tissues and brain regions involved cardiovascular regulation, II causes mitochondrial dysfunction is often accompanied by morphological changes. Here we tested hypothesis Neuro‐2A cells, both functional changes mitochondria. Osmominipumps were inserted C57BL6 mice for infusion Ang‐II (600 ng/kg/min) or vehicle 14 days. Brains then harvested...
Rodent and human studies suggest that ventromedial hypothalamus (VMH) KATP channels suppress EGP. The VMH possesses glucose-sensing neurons are either excited (GE) or inhibited (GI) by glucose. Since administration of the channel activator DZ reduces EGP in rodents humans, we examined impact on glucose sensing neurons. opens both plasma membrane mt channels; former inhibits while latter maintains mitochondrial metabolic function. We hypothesize concentration brain lowers affects not...
The neurodegeneration seen in Alzheimer's disease (AD) is largely attributed to the over‐production and accumulation of protein Amyloid beta (Aβ), which becomes toxic cells induces dysfunction cellular organelles inflict damage. Recent publications have demonstrated that epoxide derivatives arachidonic acid, epoxyeicosatrienoic acids (EETs; 14,15‐, 11,12‐, 8,9‐ 5,6‐EET), are cytoprotective brain promote neuronal growth. involvement EETs AD has not been studied yet. Our previous data suggests...