ArticleMolecular endocrinology (Baltimore, Md.)2009
Connective tissue growth factor (CTGF) inactivation leads to defects in islet cell lineage allocation and beta-cell proliferation during embryogenesis.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
56 citing papers in PubMed, 81 citations in OpenAlex.
- The stem cell within the vessel wall: multipotent pericytes modulating β-cell function and diabetic complications.Stem cell research & therapy · 2025Review
- The role of endothelial cells in pancreatic islet development, transplantation and culture.Frontiers in cell and developmental biology · 2025Review
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- Context-dependent effects of CCN2 on β-cell mass expansion and indicators of cell stress in the setting of acute and chronic stress.American journal of physiology. Endocrinology and metabolism · 2023Article
- Recent progress on the role of cellular communication network factors (CCN) 3, 4 and 6 in regulating adiposity, liver fibrosis and pancreatic islets.Journal of cell communication and signaling · 2023Review
- Review
- TEAD1 regulates cell proliferation through a pocket-independent transcription repression mechanism.Nucleic acids research · 2022Article
- Multifunctional regulatory protein connective tissue growth factor (CTGF): A potential therapeutic target for diverse diseases.Acta pharmaceutica Sinica. B · 2022Review
- Metabolic Effects of CCN5/WISP2 Gene Deficiency and Transgenic Overexpression in Mice.International journal of molecular sciences · 2021Review
- Recapitulating pancreatic cell-cell interactions through bioengineering approaches: the momentous role of non-epithelial cells for diabetes cell therapy.Cellular and molecular life sciences : CMLS · 2021Review
- Reduced synchroneity of intra-islet CaeLife · 2021Article
- CCN2/CTGF promotor activity in the developing and adult mouse eye.Cell and tissue research · 2021Article
- An Overview of Engineered Hydrogel-Based Biomaterials for ImprovedFrontiers in bioengineering and biotechnology · 2021Review
- The Role of Vascular Cells in Pancreatic Beta-Cell Function.Frontiers in endocrinology · 2021Review
- Emerging Roles of Vascular Endothelium in Metabolic Homeostasis.Circulation research · 2018Review
- Development of Normal and Cleft Palate: A Central Role for Connective Tissue Growth Factor (CTGF)/CCN2.Journal of developmental biology · 2018Review
- Degradation of the endoplasmic reticulum-anchored transcription factor MyRF by the ubiquitin ligase SCFThe Journal of biological chemistry · 2018Article
- Regulation and bioactivity of the CCN family of genes and proteins in obesity and diabetes.Journal of cell communication and signaling · 2018Review
- Virus-like infection induces human β cell dedifferentiation.JCI insight · 2018Article
- Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The factors necessary for normal pancreatic islet morphogenesis have not been well characterized. Here we report that connective tissue growth factor (CTGF) is involved in the establishment of normal islet endocrine cell ratio and architecture. CTGF is a secreted protein known to modulate several growth factor-signaling pathways including TGF-beta, BMP, and Wnt. Although its role in pancreatic diseases such as pancreatitis and pancreatic cancer are well documented, a role for CTGF in normal pancreas development and function has heretofore not been examined. Using a lacZ-tagged CTGF allele, we describe for the first time the expression pattern of CTGF in the developing pancreas and the requirement of CTGF for normal islet morphogenesis and embryonic beta-cell proliferation. CTGF is highly expressed in pancreatic ductal epithelium and vascular endothelium, as well as at lower levels in developing insulin(+) cells, but becomes down-regulated in beta-cells soon after birth. Pancreata from CTGF null embryos have an increase in glucagon(+) cells with a concomitant decrease in insulin(+) cells, and show defects in islet morphogenesis. Loss of CTGF also results in a dramatic decrease in beta-cell proliferation at late gestation. Unlike CTGF null embryos, CTGF heterozygotes survive past birth and exhibit a range of islet phenotypes, including an intermingling of islet cell types, increased number of glucagon(+) cells, and beta-cell hypertrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.