Biglycan, a small leucine-rich proteoglycan (SLRP), is a crucial component of the extracellular matrix (ECM) associated with the maintenance of tissue homeostasis. In response to tissue damage, the ECM-derived soluble form of biglycan acts as a danger signal by triggering an inflammatory response via the toll-like receptor (TLR)2/TLR4 in macrophages and dendritic cells. The impact and signaling mechanism of biglycan in innate immunity is better understood with the use of specific and reliable research tools and investigation techniques. Accordingly, our lab has established explicit and detailed experimental protocols to examine the in vitro and in vivo effects of biglycan in cellular immune responses. To evaluate the in vitro effects of biglycan on macrophage activation, a comprehensive protocol that makes use of murine peritoneal macrophages has been described. Further, to study the in vivo effects of biglycan, a method that uses a pLIVE vector to generate transgenic mice transiently overexpressing human biglycan is detailed. A step-by-step protocol for analyzing the effects of soluble biglycan overexpression in transgenic mice is explained under the following sections: (1) construction of pLIVE-hBGN plasmid, (2) intravenous delivery of transgenic vector, (3) identification of hBGN transgene in hepatocytes (4) detection of transgenic biglycan protein in the plasma of transgenic mice, and (5) evaluation of the presence and pro-inflammatory effects of transgenic biglycan in extrahepatic mouse tissues.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-1-0716-2946-8_9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Biglycan stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes.
FASEB J
January 2025
Department of Ophthalmology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Article Synopsis
- Retinal pathological angiogenesis (PA) is linked to diseases like age-related macular degeneration and diabetic retinopathy, and this study explores the role of the protein biglycan (BGN) in this process using a mouse model.
- The researchers found that BGN levels increased in the retinas of mice with oxygen-induced retinopathy and that inhibiting BGN led to reduced PA, suggesting BGN plays a crucial role in promoting this condition.
- Further analysis indicated that BGN's effect on PA may involve the upregulation of another protein, CXCL12, and blocking the interaction between CXCL12 and its receptor significantly decreased PA in mice, highlighting the importance of pericytes in
Decorin Knockdown Improves Aged Tendon Healing by Enhancing Recovery of Viscoelastic Properties, While Biglycan May Not.
Ann Biomed Eng
November 2024
McKay Orthopaedic Research Laboratory, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
The objective of the study was to determine the specific roles of decorin and biglycan in the early and late phases of tendon healing in aged mice. Aged (300 day-old) female wildtype (WT), Dcn (I-Dcn), Bgn (I-Bgn), and compound Dcn/Bgn (I-Dcn/Bgn) mice with a tamoxifen (TM) inducible Cre underwent a bilateral patellar tendon injury (PT). Cre excision of the conditional alleles was induced at 5 days (samples collected at 3 and 6 weeks) or 21 days post-injury (samples collected at 6 weeks).
View Article and Find Full Text PDFPDK1 promotes epithelial ovarian cancer progression by upregulating BGN.
Acta Biochim Biophys Sin (Shanghai)
November 2024
Department of Laboratory Medicine, the First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Pyruvate dehydrogenase kinase 1 (PDK1) is a new therapeutic target that is dysregulated in multiple tumors. This study aims to explore the potential role and regulatory mechanism of PDK1 in epithelial ovarian cancer (EOC). We detect PDK1 expression in EOC tissues and cells using qRT-PCR and western blot analysis, and the effects of PDK1 on EOC cell malignant behaviors are explored.
View Article and Find Full Text PDFRole of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis.
BMC Oral Health
November 2024
Department of Periodontal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.
Article Synopsis
- This study investigates the mechanisms behind idiopathic gingival fibromatosis (IGF) by analyzing human gingival fibroblasts (hGFs) from affected patients.
- RNA sequencing revealed that in IGF, there is a decrease in transglutaminase 2 (TGM2) and an increase in biglycan (BGN) compared to those with periodontitis.
- The research found that inhibiting specific protein (SP)1 reduces BGN expression, suggesting that SP1 promotes BGN elevation and consequently leads to TGM2 suppression in IGF.
DAMPs Drive Fibroinflammatory Changes in the Glaucomatous ONH.
Invest Ophthalmol Vis Sci
October 2024
University of Wisconsin-Madison, Madison, Wisconsin, United States.
Article Synopsis
- - The study investigates the early molecular mechanisms behind glaucoma, focusing on B6.EDA+/+ mice, which express a damage-associated molecule (FN+EDA) that triggers an inflammatory response in the optic nerve head.
- - Researchers found that these mice experience significantly higher intraocular pressure and retinal damage compared to control mice, with increased expression of proteins like FN+EDA and biglycan linked to these changes.
- - Gene analysis and protein expression studies over two years revealed new molecular pathways related to glaucomatous damage, highlighting the role of FN+EDA in promoting inflammation in the optic nerve head as the mice aged.
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!