Retinoid Machinery in Distinct Neural Stem Cell Populations with Different Retinoid Responsiveness

Orsolits, Barbara; Borsy, Adrienn; Madarász, Emı́lia; Mészáros, Z.; Köhidi, Tímea; Markó, Károly; Jelitai, Márta; Welker, Ervin; Környei, Zsuzsanna

doi:10.1089/scd.2012.0422

Cited by 14 publications

(16 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…48 Both lecithin retinol acyltransferase and mesoderm posterior 1 homolog, which are suggested to be specifically expressed by HSCs or their precursors, are also expressed by embryonic and adult stem cells from mice and humans. 49,50 Transplanted HSCs contribute to liver regeneration in host animals by forming mesenchymal tissue, progenitor cells, hepatocytes, and cholangiocytes. 51 HSCs contribute to the formation of K19 þ and a-fetoproteinepositive cells during DRs in vivo, thus sustaining the notion that mesenchymal cells that surround DRs may not only influence the differentiation of progenitor cells, but also contribute to their population.…”

Section: Hscs Contribute To Hpcs and Vice Versamentioning

confidence: 99%

Hepatic Progenitor Cells in Action

Kaur

Siddiqui

Bhat

2015

The American Journal of Pathology

View full text Add to dashboard Cite

Liver injury caused by drugs, viruses, and toxins that impede the proliferation of mature hepatocytes results in the activation of hepatic progenitor cells (HPCs), which then participate in the restoration of the damaged liver tissue. HPCs are known to be bipotential cells, capable of forming both hepatocytes and cholangiocytes when regeneration by mature hepatocytes is plagued or impaired. Both clinical studies of liver disease and certain experimental animal models of liver injury conspicuously show the presence of activated HPC response and proliferation. However, in addition to regeneration, the proliferation of HPCs also determines the appearance of a ductular reaction that has been correlated with progressive portal fibrosis, suggesting intricate links between activation of HPCs and fibrogenesis. The current review highlights the role of activated HPCs in both hepatic regeneration and fibrosis during liver injury.

show abstract

Section: Hscs Contribute To Hpcs and Vice Versamentioning

confidence: 99%

Hepatic Progenitor Cells in Action

Kaur

Siddiqui

Bhat

2015

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Interestingly, LRAT and MESP1, which are suggested to be specifically expressed by HSCs or their precursors (20,21), are expressed by embryonic and adult stem cells from mice and humans (Embryonic Stem Cell Database, http://biit.cs.ut.ee/ escd/; refs. 22,23). Owing to these opposing lineage-tracing studies, we performed cell transplantation experiments with HSCs in the present study to determine their contribution to liver regeneration.…”

Section: Introductionmentioning

confidence: 99%

Hepatic stellate cells contribute to progenitor cells and liver regeneration

Kordes¹,

Sawitza²,

Götze³

et al. 2014

J. Clin. Invest.

147

112

View full text Add to dashboard Cite

“…The molecular genetic evidence based on loss of gene activity proposes a connection between retinoic acid signaling and the normal formation of the forebrain and head, in particular a head promoting role, mainly during gastrula stages. Additional studies have identified multiple roles for retinoic acid during neurogenesis, cortex development, retina formation, and many others (Halilagic et al, 2007;Haushalter, Asselin, Fraulob, Dollé, & Rhinn, 2017;Lupo et al, 2005;Massimino et al, 2018;Orsolits et al, 2013;Siegenthaler et al, 2009;Suzuki et al, 2000). Some of the phenotypes of these additional retinoic acid functions could give rise to head malformations and microcephaly.…”

Section: Retinoic Acid Affects Forebrain Morphogenesis Resulting Inmentioning

confidence: 99%

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Petrelli

Bendelac

Hicks

et al. 2019

Genesis

View full text Add to dashboard Cite

Summary Fetal Alcohol Spectrum Disorder (FASD) is a set of neurodevelopmental malformations caused by maternal consumption of alcohol during pregnancy. FASD sentinel facial features are unique to the disorder, and microcephaly is common in severe forms of FASD. Retinoic acid deficiency has been shown to cause craniofacial malformations and microcephaly in animal models reminiscent of those caused by prenatal alcohol exposure. Alcohol exposure affects the migration and survival of cranial neural crest cells, which are required for proper frontonasal prominence and pharyngeal arch development. Defects in craniofacial development are further amplified by the many downstream pathways that are transcriptionally controlled retinoic acid target genes, including Shh signaling. Recent evidence shows that alcohol exposure itself is sufficient to induce retinoic acid deficiency in the embryo. These data suggest that retinoic acid deficiency is an important underlying etiology of FASD. In disorders like Vitamin A Deficiency, FASD, DiGeorge (22q11.2 Deletion Syndrome), CHARGE, Smith‐Magenis, Matthew‐Wood, and Congenital Zika Syndromes, evidence is accumulating to link reduced retinoic acid signaling with developmental defects like craniofacial malformations and microcephaly. Research focus on characterizing the effects of retinoic acid deficiency during early development and on understanding the downstream signaling pathways involved in aberrant head, and craniofacial development will reveal underlying etiologies of these disorders.

show abstract

Retinoid Machinery in Distinct Neural Stem Cell Populations with Different Retinoid Responsiveness

Cited by 14 publications

References 61 publications

Hepatic Progenitor Cells in Action

Hepatic Progenitor Cells in Action

Hepatic stellate cells contribute to progenitor cells and liver regeneration

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Contact Info

Product

Resources

About