Biology subjects

Hernandez, J. L.

Publications and source records attributed to Hernandez, J. L..

3 recordsLinked to original sources

bioRxiv2026

Fibroblast signaling influences macrophage-dependent, biomaterial-induced tissue remodeling

The ability to induce tissue regeneration on demand using biomaterials remains a major goal in biomedical research, yet significant challenges persist. Among the most advanced biomaterial models, the nanofiber-hydrogel composite has demonstrated a striking ability to induce soft adipose tissue remodeling at the injection site without incorporating exogenous biological cues.1,2 However, the underlying mechanisms that drive such a tissue response remain unclear. Here, we show that biomaterial-induced tissue remodeling is driven by sustained and controlled inflammation mediated by macrophages in strong communication with fibroblasts. Notably, both pro-inflammatory and anti-inflammatory signals remained elevated during this process in the long-term, challenging the prevailing notion that inflammation opposes remodeling. Using macrophage depletion in mice, we demonstrate that macrophages are essential for this process. Single-cell RNA sequencing further revealed robust fibroblast-to-macrophage signaling, contrasting with the conventional macrophage-to-fibroblast paradigm, and identified unique Spp1 macrophages and Ctla2a fibroblasts within the remodeling niche. These findings provide a comprehensive view of the immune landscape in biomaterial-induced tissue remodeling, highlighting key cellular interactions, prolonged kinetics, and unexpected signaling pathways. By defining key targets and fundamental principles, this work has broad implications for advancing biomaterial-induced tissue regeneration.

bioengineering↗

bioRxiv2024

Immunologic comparisons of strain and induction method in an improved mouse model of intrauterine fibrosis

Intrauterine adhesions are growths of fibrotic tissue within the uterine cavity and can arise from a variety of tissue-damaging stimuli. Immune cells are known to mediate fibrotic responses, but specific mechanisms require further elucidation. Here, we compared intrauterine fibrosis development and immune responses across different mouse strains and induction methods. We aimed to identify a consistent and more clinically relevant mouse model of intrauterine fibrosis, whether immune responses differ in response to different stimuli, and which potential key immune cell populations are responsible for intrauterine fibrosis susceptibility. Intrauterine fibrosis induction methods were compared using surgical curettage or transcervically administered chemical (quinacrine) models. Measurements of tissue morphology and collagen gene expression indicate BALB/c mice are more susceptible than C57BL/6 mice to intrauterine fibrosis. In chemically induced BALB/c uterine tissues, gene expression and flow cytometry data show greater pro-inflammatory macrophage responses, implicating a possible role in fibrogenesis consistent with human intrauterine adhesion data. Findings from this study demonstrate the importance of mouse strain selection in studies of intrauterine adhesions. Furthermore, we show that a new hormone-synchronized, chemically induced mouse model can more uniformly and reliably provoke fibrotic tissue response. This model may allow for greater elucidation of mechanisms involved in intrauterine adhesion development, and exploratory therapeutic studies for treatment intervention.

bioengineering↗

bioRxiv2020

Independent Tryptophan pathway in Trichoderma asperellum and T koningiopsis: New insights with bioinformatic and molecular analysis

The synthesis of Indole Acetic Acid from tryptophan has been described in plants, fungi and bacteria; it is thus known as tryptophan-dependent indole acetic acid. Four possible pathways of IAA formation have been described, including the indole acetonitrile acid (IAN), indole acetamide (IAM), indole-pyruvic (IAP) and tryptamine (TRM) pathways. Of these, the indole acetonitrile pathway is particularly important because when this compound is transformed into IAA, a nitrogenated molecule is released. The microorganisms that have this pathway are thus called nitrogen fixers. There is another little-studied pathway called TRP-Independent, so-called because the IAA that is formed in it can have an exogenous origin, chorismic acid (CHA), and it enters the pathway through anthranilic acid (ANA). The TRP-Independent pathway is made up of three stages. The first from CHA to ANA, the second from AA to IAA and the third from TRP to ANA through Kynurenine (KYN). This work describes the different stages of the pathway, as well as the enzymes and the genes that control the production of IAA, using a bioinformatic analysis of the genes involved, which were identified by PCR. An expression analysis showed that only T asperellum has the necessary genes to incorporate ANA into the TRP-I pathway and synthesize IAA through it. The analysis also detected the gene that regulates anthranilate phosphoribosyl transferase (AFT), an enzyme necessary for the synthesis of AIA from ANA; the presence of this gene was confirmed in the two species analyzed.

microbiology↗