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Biology subjects

Ahmed, M. S.

Publications and source records attributed to Ahmed, M. S..

7 recordsLinked to original sources

Eph-Ephrin Tetramerization Inhibitors Target Bidirectional Signaling to Combat Pain and Addiction

Eph receptors and Ephrin ligands are a large highly conserved family of interacting membrane-anchored molecules that form dimers, tetramers, and tetramer superclusters to become activated and signal upon cell-cell contact. While most noted for their ability to transduce bidirectional phosphotyrosine signals in development, certain Ephs and Ephrins also become overexpressed and participate in pathological situations, including EphB1 in chronic pain/addiction and EphB2 in fibroinflammatory disorders and cancer. We searched for small molecules that disrupt EphB-EphrinB receptor-ligand interactions and discovered compounds with submicromolar activity that specifically inhibit formation of the tetramer. Compounds effectively target tetramer-driven EphB1-EphrinB2 and EphB2-EphrinB2 interactions, while showing less action towards the more dimer-driven EphB4-EphrinB2 interaction. They are orally available, exhibit drug-like qualities to reduce both EphB forward and EphrinB reverse signaling, and act to blunt inflammatory pain and opioid withdrawal behaviors. Tetramer inhibitors thus present a novel way to target Eph-Ephrin macromolecular interactions and counter pathologies caused or exacerbated by excessive bidirectional signaling.

molecular biology↗

Pan-EphB tyrosine kinase inhibitor mitigates diabetic cardiomyopathy

Diabetic cardiomyopathy (DCM) is characterized by myocardial fibrosis, excessive collagen deposition, decline in ejection fraction and diastolic dysfunction in diabetic subjects. As current pharmaceuticals have varying efficacy and adverse effects, there is an unmet need for new therapeutics. We recently identified STA-013, a pan-EphB tyrosine kinase inhibitor sparing EphB3, that resulted in whole-body weight loss, restored glucose homeostasis, and mitigated insulin resistance in diet-induced obese mouse models. Here, we now show in a streptozotocin (STZ)-high-fat diet-induced mouse model that STA-013 decreased body weight and restored glucose homeostasis while mitigating insulin resistance. Importantly, STA-013 significantly improved cardiac function in part by increasing ejection fraction and fractional shortening, and reduced collagen deposition suggestive of decreased cardiac fibrosis. This was associated with a significant downregulation of key molecular intermediaries including phosphorylation EphB tyrosine kinase signaling, insulin receptor signal, and TGF-{beta} levels in STA-013 treated STZ-HFD mice. Together, our preclinical findings support the development of pan-EphB tyrosine kinase inhibitors as novel therapeutics to mitigate DCM and associated complications.

pharmacology and toxicology↗

Study of Plasma Adiponectin Levels in Patients with Metabolic Syndrome and Therapeutic Indication in Bangladesh

BackgroundThe metabolic syndrome (Met-S) is a cluster of some interrelated common clinical disorders, including central obesity, dyslipidemia, hypertension, and glucose intolerance. Central obesity, accompanied by insulin resistance, is a key factor for the development of metabolic syndrome. Adiponectin is an adipose-specific plasma protein, secreted from adipocyte with anti-atherogenic and insulin-sensitizing activities. PurposeThis study aimed to investigate the relationship of plasma adiponectin levels with metabolic syndrome, related disorders and its drug repurposing through in silico approach. Materials and MethodsFor this study, 269 individuals were recruited with written consent. The participants were selected based on their full medical history, clinical examination, and laboratory reports. Anthropometric measurements as well as blood pressure was measured before sample collection. Fasting blood samples were collected for the estimation of lipid profile, blood glucose, and serum adiponectin levels. ResultsOur results show that the adiponectin levels in the subjects with Met-S were significantly lower than those of without Met-S (p <0.0001). Among the metabolic syndrome risk factors, adiponectin levels were associated with hypertriglyceridemia and reduced HDL-cholesterol (p<0.0001). Three drugs (Saquinavir, Candesartan and Glimepiride) were suggested to control the plasma adiponectin level in the subjects with Met-S. ConclusionsSince the plasma adiponectin levels are significantly lower in patients with Met-S, it might be used as diagnostic & prognostic marker for Met-S disorder and adiponectin targeted drugs might be minimize the Met-S of the subjects.

biochemistry↗

Arrestin-3-assisted activation of JNK3 mediates dopaminergic behavioral and signaling plasticity in vivo.

In rodents with unilateral ablation of the substantia nigra neurons supplying dopamine to the striatum, chronic treatment with the dopamine precursor L-DOPA or dopamine agonists induces a progressive increase of behavioral responses, a process known as behavioral sensitization. The sensitization is blunted in arrestin-3 knockout mice. Using virus-mediated gene delivery to the dopamine-depleted striatum of arrestin-3 knockout mice, we found that the restoration of arrestin-3 fully rescued behavioral sensitization, whereas its mutant defective in JNK activation did not. A 25-residue arrestin-3-derived peptide that facilitates JNK3 activation in cells, expressed ubiquitously or selectively in the direct pathway striatal neurons, fully rescued sensitization, whereas an inactive homologous arrestin-2-derived peptide did not. Behavioral rescue was accompanied by the restoration of JNK3 activity and of JNK-dependent phosphorylation of the transcription factor c-Jun in the dopamine-depleted striatum. Thus, arrestin-3-dependent JNK3 activation in direct pathway neurons is a critical element of the molecular mechanism underlying sensitization.

neuroscience↗

Structural Insights of SARS-CoV-2 Spike Protein from Delta and Omicron Variants

Given the continuing heavy toll of the COVID-19 pandemic and the emergence of the Delta (B.1.617.2) and Omicron (B.1.1.529) variants, the WHO declared both as variants of concern (VOC). There are valid concerns that the latest Omicron variant might have increased infectivity and pathogenicity. In addition, the sheer number of S protein mutations in the Omicron variant raise concerns of potential immune evasion and resistance to therapeutics such as monoclonal antibodies. However, structural insights that underpin the potential increased pathogenicity are unknown. Here we adopted an artificial intelligence (AI)-based approach to predict the structural changes induced by mutations of the Delta and Omicron variants in the spike (S) protein using Alphafold. This was followed by docking the human angiotensin-converting enzyme 2 (ACE2) with the predicted S proteins for Wuhan-Hu-1, Delta, and Omicron variants. Our in-silico structural analysis indicates that S protein for Omicron variant has a higher binding affinity to ACE-2 receptor, compared to Wuhan-Hu-1 and Delta variants. In addition, the recognition sites of the receptor binding domains for Delta and Omicron variants showed lower electronegativity compared to Wuhan-Hu-1. Importantly, further molecular insights revealed significant changes induced at fusion protein (FP) site, which may mediate enhanced viral entry. These results represent the first computational analysis of structural changes associated with Omicron variant using Alphafold, Collectively, our results highlight potential structural basis for enhanced pathogenicity of the Omicron variant, however further validation using X-ray crystallography and cryo-EM are warranted.

biophysics↗

Hippocampal network reorganization underlies the formation of a temporal association memory

Episodic memory requires linking events in time, a function dependent on the hippocampus. In \"trace\" fear conditioning, animals learn to associate a neutral cue with an aversive stimulus despite their separation in time by a delay period on the order of tens of seconds. But how this temporal association forms remains unclear. Here we use 2-photon calcium imaging to track neural population dynamics over the complete time-course of learning and show that, in contrast to previous theories, the hippocampus does not generate persistent activity to bridge the time delay. Instead, learning is concomitant with broad changes in the active neural population in CA1. While neural responses were highly stochastic in time, cue identity could be reliably read out from population activity rates over longer timescales after learning. These results question the ubiquity of neural sequences during temporal association learning, and suggest that trace fear conditioning relies on mechanisms that differ from persistent activity accounts of working memory.

neuroscience↗

Macrophage-derived granulin drives resistance to immune checkpoint inhibition in metastatic pancreatic cancer

The ability of disseminated cancer cells to evade the immune response is a critical step for efficient metastatic progression. Protection against an immune attack is often provided by the tumour microenvironment that suppresses and/or excludes cytotoxic CD8+ T cells. Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive metastatic disease with unmet needs, yet the immuno-protective role of the metastatic tumour microenvironment in pancreatic cancer is not completely understood. In this study we find that macrophage-derived granulin contributes to cytotoxic CD8+ T cell exclusion in metastatic livers. Mechanistically, we find that granulin expression by macrophages is induced in response to colony stimulating factor-1. Genetic depletion of granulin reduces the formation a fibrotic stroma, thereby allowing T cell entry at the metastatic site. While metastatic PDAC tumours are largely resistant to anti-PD-1 therapy, blockade of PD-1 in granulin depleted tumours restored the anti-tumour immune defence and dramatically decreased metastatic tumour burden. These findings suggest that targeting granulin may serve as a potential therapeutic strategy to restore CD8+ T cell infiltration in metastatic PDAC, thereby converting PDAC metastatic tumours, which are refractory to immune checkpoint inhibitors, into tumours that respond to immune checkpoint inhibition therapies.

cancer biology↗