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Biology subjects

Kidd, M.

Publications and source records attributed to Kidd, M..

3 recordsLinked to original sources

Direct interoceptive input to the insular cortex shapes learned feeding behavior

The insular cortex (insula) is an interoceptive hub, which senses internal states such as hunger, thirst, pain, and emotions. Previous studies suggest that the insula directly senses internal states, but the mechanisms remain elusive. We identified a population of leptin receptor-positive cells with a unique morphology in the insula (INSLepR). Based on leptins known role in signaling adiposity, we hypothesized that INSLepR neurons detect internal states to regulate food intake and body weight. Accordingly, we found that intra-insula leptin administration or optogenetic stimulation of INSLepR neurons impacts feeding behavior. Moreover, INSLepR neuron activity encodes feeding bouts in an internal-state dependent manner, and leptin alters insula neural dynamics in response to feeding, while also reshaping the transcriptome. Taken together, our data supports a model for direct interoceptive input to the insula, in which INSLepR cells integrate adiposity level signals to regulate feeding and body weight in a learned manner.

neuroscience↗

Loss of cytoskeletal proteostasis links dysregulation of cell size and mechanotransduction in mesenchymal stem cell senescence

Tissues are maintained by homeostatic feedback mechanisms where cells respond to, but also modify, the chemical and mechanical properties of the surrounding extracellular matrix. Mesenchymal stem cells (MSCs) resident in the marrow niche experience a diverse mechanical environment, but ageing can affect the composition and quality of bone and marrow tissues. Here we quantified the effect of replication-induced senescence on MSC morphology and their ability to correctly respond to different substrate stiffnesses. The matrix proteome was found to be sensitive to substrate stiffness, but pharmacological inhibition of cellular contractility perturbed this response, decreasing levels of tenascin-C, fibulins and fibronectin. Similar decreases in these mechanosensitive proteins were observed in senescent cells, suggested a decoupling of mechanotransduction pathways. Intracellular proteomic and transcriptomic analyses confirmed a decrease in components of the cytoskeletal chaperone complex CCT/TRiC in senescent MSCs. Finally, pharmacological inhibition of CCT/TRiC was able to partially recapitulate senescence-associated morphological changes in non-senescent MSCs. These results demonstrate a senescence-mediated perturbation to cytoskeletal homeostasis, pathways of mechanotransduction and the secretion of matrix proteins required for tissue maintenance.

cell biology↗

Vimentin is Required for Tumor Progression and Metastasis in a Mouse Model of Non-Small Cell Lung Cancer

Vimentin, a type III intermediate filament, is highly expressed in aggressive epithelial cancers and is associated with increased rates of metastasis. We show that vimentin is causally required for lung cancer metastasis using a genetic mouse model of lung adenocarcinoma (LSL-KrasG12D;Tp53fl/fl, termed KPV+/+) crossed with vimentin-null mice (thereby creating KPV-/- mice). Both KPV+/+ and KPV-/- mice developed lung tumors, yet KPV-/- mice had delayed tumorigenesis and prolonged survival. KPV+/+ cells implanted in the flank metastasized to the lung while KPV-/- cells did not, providing additional evidence that vimentin is required for metastasis. Differential expression analysis of RNA-seq data demonstrated that KPV-/- cells had suppressed expression of genes that drive epithelial-to-mesenchymal transition, migration, and invasion, processes that are critical to the metastatic cascade. Integrative metabolomic and transcriptomic analysis revealed altered glutaminolysis, with KPV-/- cells accumulating glutathione, leading to impaired cell motility in response to oxidative stress. Together, these results show that loss of vimentin impairs epithelial-to-mesenchymal transition and regulation of the oxidative stress response, resulting in decreased metastasis in murine lung adenocarcinoma.

cancer biology↗