PubMed Health⌕ Search

PubMed · 14999680

Gene expression pattern in hepatic stem/progenitor cells during rat fetal development using complementary DNA microarrays.

Abstract

To identify new and differentially expressed genes in rat fetal liver epithelial stem/progenitor cells during their proliferation, lineage commitment, and differentiation, we used a high throughput method-mouse complementary DNA (cDNA) microarrays-for analysis of gene expression. The gene expression pattern of rat hepatic cells was studied during their differentiation in vivo: from embryonic day (ED) 13 until adulthood. The differentially regulated genes were grouped into two clusters: a cluster of up-regulated genes comprised of 281 clones and a cluster of down-regulated genes comprised of 230 members. The expression of the latter increased abruptly between ED 16 and ED 17. Many of the overexpressed genes from the first cluster fall into distinct, differentially expressed functional groups: genes related to development, morphogenesis, and differentiation; calcium- and phospholipid-binding proteins and signal transducers; and cell adhesion, migration, and matrix proteins. Several other functional groups of genes that are initially down-regulated, then increase during development, also emerged: genes related to inflammation, blood coagulation, detoxification, serum proteins, amino acids, lipids, and carbohydrate metabolism. Twenty-eight genes overexpressed in fetal liver that were not detected in adult liver are suggested as potential markers for identification of liver progenitor cells. In conclusion, our data show that the gene expression program of fetal hepatoblasts differs profoundly from that of adult hepatocytes and that it is regulated in a specific manner with a major switch at ED 16 to 17, marking a dramatic change in the gene expression program during the transition of fetal liver progenitor cells from an undifferentiated to a differentiated state. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Petko M Petkov, Jiri Zavadil, David Goetz, Tearina Chu, Robert Carver, Charles E Rogler, Erwin P Bottinger, David A Shafritz, Mariana D Dabeva. 2004. Gene expression pattern in hepatic stem/progenitor cells during rat fetal development using complementary DNA microarrays.. https://doi.org/10.1002/hep.20088

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

An open benchmark and language models for AI in aging biology.

Over the past two decades, human aging has been characterized across DNA methylation, transcriptomic, proteomic, and clinical modalities, yet no benchmark evaluates whether AI systems can interpret these heterogeneous data types in the context of aging biology. We introduce LongevityBench, an open suite of 17 tasks spanning five biodata domains, and use it to assess 18 frontier AI systems from six developer teams. Despite recent advances in AI, no single model dominates all tasks, with omics-based age prediction being the hardest task regardless of scale. To test whether these gaps can be closed without frontier-scale resources, we fine-tuned a family of five multitask Longevity-LLMs on domain-specific aging data. The compact (0.6B-9B parameters) Longevity-LLMs matched or exceeded far larger frontier systems on LongevityBench, showing that general-purpose language models can be adapted to structured-omics tasks. We publicly release the benchmark, models, and Longevity Claw, an agentic research interface for aging researchers.

Aging↗

Association between sirtuin 1 and markers of oxidative stress in master athletes.

BACKGROUND: Lifelong training in master athletes confers protective effects, promoting higher sirtuin levels and enhanced antioxidant capacity. Although Sirtuin 1 (SIRT1) is well studied, no previous study has examined the relationship between circulating SIRT1 levels and antioxidant defense variables in master athletes. PURPOSE: To compare and analyze the relationships between circulating levels of SIRT1 and variables related to antioxidant defense in master athletes (MA) and untrained middle-aged individuals (UMA). METHODS: Male MA (n&#x2009;=&#x2009;42; 51.62&#x2009;&#xb1;&#x2009;7.33 years; &#x2265;10 years of training and competition in running) and UMA (n&#x2009;=&#x2009;15; 47.73&#x2009;&#xb1;&#x2009;8.52 years) were evaluated. Venous blood samples were collected for biochemical analyses of SIRT1, antioxidant enzymes, TBARS and F2-isoprostanes, 8-OHdG, and redox balance indexes. RESULTS: MA showed higher levels of SIRT1 (18.22&#x2009;&#xb1;&#x2009;4.53 vs. 6.08&#x2009;&#xb1;&#x2009;2.11 ng/mL; p&#x2009;<&#x2009;0.0001), as well as of SOD, CAT, and GSH (p&#x2009;<&#x2009;0.001), indicating a more favorable antioxidant profile. After adjustment for body fat percentage, differences in SOD, CAT, GSH and TBARS, remained significant. SIRT1 was positively correlated with SOD (r&#x2009;=&#x2009;0.279; p&#x2009;=&#x2009;0.031), CAT (r&#x2009;=&#x2009;0.485; p&#x2009;<&#x2009;0.001), GSH (r&#x2009;=&#x2009;0.476; p&#x2009;<&#x2009;0.001) and CAT/8-OHdG (r&#x2009;=&#x2009;0.430; p&#x2009;=&#x2009;0.032), and negatively correlated with TBARS (r&#x2009;=&#x2009;-&#x2009;0.518; p&#x2009;<&#x2009;0.001). CONCLUSION: Master athletes exhibited higher circulating SIRT1 concentrations and a more favorable systemic redox profile than untrained individuals, with SIRT1 being associated with markers of antioxidant defense, lipid peroxidation, and redox balance.

Aging↗

Decoding SUMOylation as a metabolic stress sensor in aging and age-related disorders: Mechanisms, tissue specificity and therapeutic potential.

SUMOylation is a reversible post-translational modification increasingly recognized for its role in coordinating cellular responses to metabolic stress during aging. Emerging evidence indicates that it functions beyond a conventional modification, representing an adaptive stress&#x2011;responsive regulatory network that integrates metabolic, oxidative, inflammatory, and proteotoxic signals. Rather than acting on isolated pathways, this network finely tunes mitochondrial function, proteostasis, genome maintenance, immune balance, and epigenetic regulation. Accumulating evidence indicates that SUMO-dependent regulation exhibits remarkable tissue specificity, supporting mitochondrial adaptation and contractile integrity in skeletal muscle, shaping lipid and glucose metabolism in the liver, modulating proteotoxic stress and neuronal resilience in the brain, and contributing to immune cell differentiation and chronic low-grade inflammation during aging. In this review, we summarize current mechanistic insights into SUMO signaling across aging-relevant tissues, with particular emphasis on its functional interplay with other post-translational modifications, including ubiquitination and acetylation. We discuss how SUMOylation operates as a shared regulatory layer while enabling context-dependent outcomes that underlie diverse aging phenotypes and age-related disorders. Finally, we evaluate emerging translational approaches-ranging from pharmacological modulation of SUMO enzymes to lifestyle interventions such as caloric restriction and exercise-that highlight both the opportunities and challenges of targeting SUMO-regulated stress responses in aging. Together, this synthesis provides a framework for understanding how SUMOylation links metabolic stress to tissue-specific aging trajectories and therapeutic potential.

Aging↗