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Biology subjects

Marie, M. A.

Publications and source records attributed to Marie, M. A..

6 recordsLinked to original sources

Rapid odorant metabolism organizes identity- and timing-based odor representations by olfactory bulb inputs and outputs

Sensory neurons encode information about external stimuli in the form of stimulus-specific patterns of activity across their population. In the mammalian olfactory system, olfactory sensory neurons (OSNs) encode odor identity with odorant-specific combinatorial patterns that are temporally structured by inhalation. We investigated the stimulus features that determine these inhalation-linked patterns, leveraging receptor- and functionally-defined OSN populations in awake mice. We found that both the chemical tuning and temporal dynamics of many odorant-evoked responses deviate from prevailing models of receptor-ligand binding and sensitivity-based timing relationships. These deviations were well-explained by rapid metabolism of odorants within the olfactory mucosa, which generates secondary odorants that activate additional OSNs within a single breath. This process fundamentally reshapes odor representations at naturally-occurring concentrations and timescales relevant to perception. Importantly, we found that timing features robustly discriminate inhaled from metabolism-generated odorants, and that these timing differences persist at the level of olfactory bulb output. Our results suggest a novel role for inhalation-linked timing in odor coding - to disambiguate inhaled odorants from those generated internally - and raise the possibility that the nervous system may differentially process external and internally-sourced olfactory stimuli on the basis of their temporal dynamics.

neuroscience↗

Evolutionary diversity and function of odorant receptors in birds

Abstract: Odorant receptors (ORs) form among the largest gene families in vertebrates; most mammals have hundreds of intact OR genes. Although birds display diverse behavior and ecology, they were long thought to rely minimally on olfaction. We reexamine this idea by using genomic data to uncover diverse and variable OR repertoires in birds, including the nocturnal kiwi (Apteryx mantelli), which possesses the largest number of ORs known (3,750). We reveal that widespread gene conversion is shaping the evolution of bird ORs, reflecting a novel mechanism for generating functional diversity. We show that ORs are expressed in avian olfactory sensory neurons and show responses to defined, ecologically relevant odorants. Our results demonstrate the importance and functional mechanisms underlying olfaction in birds.

evolutionary biology↗

The GPR4 antagonist NE-52-QQ57 increases survival, mitigates the hyperinflammatory response and reduces viral load in SARS-CoV-2-infected K18-hACE2 transgenic mice

COVID-19 (Coronavirus disease 19) is caused by infection with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) in the respiratory system and other organ systems. Tissue injuries resulting from viral infection and host hyperinflammatory responses may lead to moderate to severe pneumonia, systemic complications, and even death. While anti-inflammatory agents have been used to treat patients with severe COVID-19, their therapeutic effects are limited. GPR4 (G protein-coupled receptor 4) is a pro-inflammatory receptor expressed on vascular endothelial cells, regulating leukocyte infiltration and inflammatory responses. In this study, we evaluated the effects of a GPR4 antagonist, NE-52-QQ57, in the SARS-CoV-2-infected K18-hACE2 transgenic mouse model. Our results demonstrated that GPR4 antagonist treatment increased the survival rate in this severe COVID-19 mouse model. The inflammatory response, characterized by proinflammatory cytokines and chemokines, was reduced in the GPR4 antagonist group compared with the vehicle group. Additionally, both SARS-CoV-2 RNA copy numbers and infectious viral titers in the mouse lung were decreased in the GPR4 antagonist group. The percentage of SARS-CoV-2 antigen-positive mouse brains was also decreased in the GPR4 antagonist group compared to the vehicle group. Furthermore, the GPR4 antagonist inhibited SARS-CoV-2 propagation in Vero E6 cells. Together, these results suggest that GPR4 antagonism may be explored as a novel approach for the treatment of COVID-19 and other similar viral diseases.

pharmacology and toxicology↗

GPR4 knockout attenuates intestinal inflammation and forestalls the development of colitis-associated colorectal cancer in murine models

GPR4 is a proton-sensing G protein-coupled receptor highly expressed in vascular endothelial cells and has been shown to potentiate intestinal inflammation in murine colitis models. Herein, we evaluated the proinflammatory role of GPR4 in the development of colitis-associated colorectal cancer (CAC) using the dextran sulfate sodium (DSS) and azoxymethane (AOM) mouse models in wild-type and GPR4 knockout mice. We found GPR4 contributed to chronic intestinal inflammation and heightened DSS/AOM-induced intestinal tumor burden. Tumor blood vessel density was markedly reduced in mice deficient in GPR4 which correlated with increased tumor necrosis and reduced tumor cell proliferation. These data demonstrate GPR4 ablation alleviates intestinal inflammation and reduces tumor angiogenesis, development, and progression in the AOM/DSS mouse model. Author summaryInflammatory bowel disease (IBD), including ulcerative colitis and Crohns disease, is a debilitating condition with chronic inflammation in the digestive tract. Patients with IBD are at higher risk of developing colitis-associated colorectal cancer (CAC), compared with the general population. The etiology of IBD is not well understood, but both genetic and environmental factors have been implicated. In this study, we investigated the role of the pH-sensing GPR4 receptor in colitis and CAC using the DSS and AOM induced mouse models. GPR4 knockout alleviated intestinal inflammation, reduced tumor angiogenesis, and impeded CAC development. Our data suggest that inhibition of GPR4 may be explored as a potential therapeutic approach for IBD treatment and CAC prevention.

cancer biology↗

The proton-sensing GPR4 receptor regulates paracellular gap formation and permeability of vascular endothelial cells

Tissue acidosis can be a consequence of numerous disease states including stroke, myocardial infarction, limb ischemia, and inflammation. Blood vessels existing in the affected tissues are associated with the progression of acidosis-related diseases. However, the mechanisms by which endothelial cells (ECs) lining the affected blood vessels sense and respond to an acidic microenvironment remain largely unclear. We investigated the functional effects of the proton-sensing G protein-coupled receptor GPR4 in acidosis-induced endothelial inflammation. GPR4 is highly expressed in ECs and known to regulate EC inflammation and endoplasmic reticulum stress responses within acidic microenvironments. Using genetic and pharmacological approaches, we demonstrate that GPR4 activation by acidosis increases EC paracellular gap formation and permeability. We further demonstrate that GPR4-mediated paracellular gap formation is dependent on the G12/13 signaling pathway. To assess the functional role of GPR4 in the inflammatory response in vivo, we utilized an acute hindlimb ischemia-reperfusion mouse model. We demonstrate that both genetic deletion and pharmacological inhibition of GPR4 reduce tissue edema, exudate formation, endothelial adhesion molecule expression, and leukocyte infiltration in the inflamed tissue. Collectively, these data suggest GPR4/G12/13 signaling mediates acidosis-induced endothelial paracellular gap formation and permeability. This study implicates GPR4 as a candidate therapeutic target for the remediation of inflammation and tissue edema.

cell biology↗

The utility of Saw-scaled viper, Echis pyramidum, and Kenyan sand boa, Eryx colubrinus as bioindicator of heavy metals bioaccumulation in relation to DPTA soil extract and biological consequences.

The present investigation was conducted to compare between the ecotoxocological effects of Ca, Mg, Fe, Cu, Zn, Co, Mo, Mn, B, Al, Sr, Pb, Ni, Cd and Cr on the saw-scaled viper, Echis pyramidum (E. p.) and the Kenyan sand boa, Eryx colubrinus (E.c.) inhabiting Gabal El-Nagar and Kahk Qibliyyah respectively in El-Faiyum desert, Egypt. Accumulation varied significantly among the liver, kidney and muscle. The relationship between concentrations of heavy metals in snakes and those in the soil from the collected sites was established by analyzing metal DPTA in soil. Bioaccumulation factor is calculated to estimate the degree of toxicity within the tissues. Morphometric analysis was recorded. All body morphometric measurements were higher in E. p. than in E. c.. Body, liver, gonad, kidney and heart weight, HSI, GSI, RBCs count, Hb content, PCV, MCV, MCH, MCHC, plasma glucose, total lipids and total proteins showed a significant increase in E. p. Histopathological examination showed damage and alterations of liver, kidney and testes sections. The tissues of E. c. were more destructed than those of E. p..

pharmacology and toxicology↗