Previous studies have shown that pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta up-regulate type VII collagen gene (COL7A1) expression in cultured dermal fibroblasts. The present study was designed to investigate the effects of TNF-alpha and IL-1beta on COL7A1 expression in epidermal keratinocytes. We demonstrated that both TNF-alpha and IL-1beta reduced COL7A1 expression in epidermal keratinocytes in an additive manner, whereas they increased COL7A1 expression in dermal fibroblasts. Thus, regulation of COL7A1 by pro-inflammatory cytokines is cell type specific. In particular, the inhibitory effects of TNF-alpha and IL-1beta occurred, at least in part, at the transcriptional level. Finally, we demonstrated that TNF-alpha and IL-1beta enhanced the TGF-beta-mediated up-regulation of COL7A1 expression in HaCaT keratinocytes, suggesting that the combination of TGF-beta and TNF-alpha or IL-1beta induces a signaling pathway that is completely different from that induced by either pro-inflammatory cytokine alone.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.0906-6705.2005.00316.xDOI Listing

Publication Analysis

Top Keywords

col7a1 expression
20
tnf-alpha il-1beta
20
pro-inflammatory cytokines
12
type vii
8
vii collagen
8
collagen gene
8
cytokines tumor
8
tumor necrosis
8
dermal fibroblasts
8
effects tnf-alpha
8

Similar Publications

Recessive dystrophic epidermolysis bullosa (RDEB) and junctional epidermolysis bullosa (JEB) are lethal blistering skin disorders resulting from mutations in genes coding for type VII collagen () and laminin 332 (, , or ), respectively. In RDEB, 25% of patients harbor nonsense mutations causing premature termination codons (PTCs). In JEB, a majority of mutations in are nonsense mutations (80%).

View Article and Find Full Text PDF

The COL7A1/PI3K/AKT axis regulates the progression of cholangiocarcinoma.

Heliyon

September 2024

Department of General Surgery, The First Affiliated Hospital of BengBu Medical College, NO. 287, Changhuai Road, Longzihu district, Bengbu, 233000, Anhui, China.

Background: The role and molecular mechanisms of collagen type VII (COL7A1) in cholangiocarcinoma (CCA) remain unknown.

Methods: We analyzed the expression of COL7A1 in CCA and its relationship with patient prognosis using bioinformatic techniques. Expression levels of COL7A1 in CCA cells and tissues were detected using reverse transcription-quantitative PCR, western blotting, and immunohistochemistry.

View Article and Find Full Text PDF

Background: To explore the abnormal metabolism-related genes that affect the prognosis of patients with lung adenocarcinoma (LUAD), and analyze the relationship with immune infiltration and competing endogenous RNA (ceRNA) network.

Methods: Transcriptome data of LUAD were downloaded from the Cancer Genome Atlas database. Abnormal metabolism-related differentially expressed genes in LUAD were screened by the R language.

View Article and Find Full Text PDF

Splice modulation strategy applied to deep intronic variants in causing recessive dystrophic epidermolysis bullosa.

Proc Natl Acad Sci U S A

August 2024

Université Paris Cité, Inserm, UMR 1163, Institut Imagine, Laboratory of Genetic Skin Diseases, Paris F-75015, France.

Recessive dystrophic epidermolysis bullosa (RDEB) is a rare and most often severe genetic disease characterized by recurrent blistering and erosions of the skin and mucous membranes after minor trauma, leading to major local and systemic complications. The disease is caused by loss-of-function variants in encoding type VII collagen (C7), the main component of anchoring fibrils, which form attachment structures stabilizing the cutaneous basement membrane zone. Alterations in C7 protein structure and/or expression lead to abnormal, rare or absent anchoring fibrils resulting in loss of dermal-epidermal adherence and skin blistering.

View Article and Find Full Text PDF

Recessive dystrophic epidermolysis bullosa (RDEB) is a rare genetic disease caused by loss of function mutations in the gene coding for collagen VII (C7) due to deficient or absent C7 expression. This disrupts structural and functional skin architecture, leading to blistering, chronic wounds, inflammation, important systemic symptoms affecting the mouth, gastrointestinal tract, cornea, and kidney function, and an increased skin cancer risk. RDEB patients have an extremely poor quality of life and often die at an early age.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!