Biology subjects

Hernandez, S. C.

Publications and source records attributed to Hernandez, S. C..

3 recordsLinked to original sources

bioRxiv2025

Fecal proteomics of wild capuchins reveals impacts of season, diet, age, and, sex on gut physiology

Understanding how the physiology of free-ranging mammals is impacted by environmental stressors is a major focus of ecological research. However, the constraints of non-invasive sampling pose serious challenges to the acquisition of physiological data from most species of primates. As a result, little is known about how the gut responds to ecological stimuli at the cellular level in wild populations. Recent research has demonstrated that proteomics could fill this knowledge gap by sequencing and quantifying proteins directly from primate feces. In order to ascertain how the gut of free-ranging white-faced capuchin monkeys (C. imitator) is influenced by environmental heterogeneity, diet, age, and sex, we sequenced 45 fecal proteomes from 24 individuals from the Sector Santa Rosa population in Costa Rica, using liquid chromatography-tandem mass spectrometry with label-free quantification. Fecal proteins assigned to C. imitator were strongly localized to gut tissues and functionally enriched for digestive and immune functions. We identified 41 capuchin candidate proteins linked to seasonality, age, sex, and diet. We also quantified abundances of dietary fruit, dietary insects, helminth gut parasites, and gut microbes. Our results demonstrate the viability of using quantitative fecal proteomics in free-ranging populations of mammals to integrate host physiology, diet, and microbial ecology through non-invasive means.

ecology↗

bioRxiv2024

Unravelling the molecular activation of the reparative cardiac fibroblasts after myocardial infarction

Activated cardiac fibroblasts (Postn+ CFs) are responsible for the healing of the heart tissue after a myocardial infarction (MI). However, so far little is known about the moment that CFs are activated, and the genes involved in this process. This is especially relevant in the context of CF heterogeneity and their role in the response to the damage. In this context, we have described a subpopulation of activated CFs responsible for the healing scar and for preventing the rupture of the ventricle after the damage: the Reparative Cardiac Fibroblasts (RCFs). Our new data indicate that RCFs directly derived from activated CFs, and this transcriptional shift happens in a close window after damage. Interestingly, our results exhibited two different molecular dynamics that would give rise to this activation and, consequently, the appearance of definitive RCFs. Using bulk RNA-Seq, RNAScope and Spatial Transcriptomics, we anatomically localized some of the genes related to both dynamics in the infarcted heart and highlight the potential role of Aspn as a new marker of this transcriptional transition in mice, pigs and patients.

bioinformatics↗

bioRxiv2019

Single-cell RNA-seq analysis reveals the crucial role of Collagen Triplex Helix Repeat Containing 1 (CTHRC1) cardiac fibroblasts for ventricular remodeling after myocardial infarction

Cardiac fibroblasts have a central role during the ventricular remodeling process associated with different types of cardiac injury. Recent studies have shown that fibroblasts do not respond homogeneously to heart damage, suggesting that the adult myocardium may contain specialized fibroblast subgroups with specific functions. Due to the limited set of bona fide fibroblast markers, a proper characterization of fibroblast population dynamics in response to cardiac damage is still missing. Using single-cell RNA-seq, we identified and characterized a fibroblast subpopulation that emerges in response to myocardial infarction (MI) in a murine model. These activated fibroblasts exhibit a clear pro-fibrotic signature, express high levels of the hormone CTHRC1 and of the immunomodulatory co-receptor CD200 and localize to the injured myocardium. Combining epigenomic profiling with functional assays, we show Sox9 and the non-canonical TGF-{beta} signaling as important regulators mediating their response to cardiac damage. We show that the absence of CTHRC1, in this activated fibroblast subpopulation, results in pronounced lethality due to ventricular rupture in a mouse model of myocardial infarction. Finally, we find evidence for the existence of similar mechanisms in a pig pre-clinical model of MI and establish a correlation between CTHRC1 levels and cardiac function after MI.

cell biology↗