scholarly journals Research Progress on Leucine-Rich Alpha-2 Glycoprotein 1: A Review

2022 ◽  
Vol 12 ◽  
Author(s):  
Yonghui Zou ◽  
Yi Xu ◽  
Xiaofeng Chen ◽  
Yaoqi Wu ◽  
Longsheng Fu ◽  
...  
Keyword(s):  
Cell Adhesion Molecules ◽  
Respiratory Diseases ◽  
Synapse Formation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Eye Diseases ◽  
Research Progress ◽  
Hematological Diseases ◽  
Endocrine Diseases ◽  
Tumor Diseases

Leucine-rich alpha⁃2 glycoprotein 1 (LRG1) is an important member of the leucine-rich repetitive sequence protein family. LRG1 was mainly involved in normal physiological activities of the nervous system, such as synapse formation, synapse growth, the development of nerve processes, neurotransmitter transfer and release, and cell adhesion molecules or ligand-binding proteins. Also, LRG1 affected the development of respiratory diseases, hematological diseases, endocrine diseases, tumor diseases, eye diseases, cardiovascular diseases, rheumatic immune diseases, infectious diseases, etc. LRG1 was a newly discovered important upstream signaling molecule of transforming growth factor⁃β (TGF⁃β) that affected various pathological processes through the TGF⁃β signaling pathway. However, research on LRG1 and its involvement in the occurrence and development of diseases was still in its infancy and the current studies were mainly focused on proteomic detection and basic animal experimental reports. We could reasonably predict that LRG1 might act as a new direction and strategy for the treatment of many diseases.

scholarly journals Molecular Mechanism of Oral Submucous Fibrosis induced by Arecoline: A Literature Review

2020 ◽  
Author(s):  
Lin Cui ◽  
Xinjia Cai ◽  
Junhui Huang ◽  
Huiling Li ◽  
Zhigang Yao
Keyword(s):  
Molecular Mechanism ◽  
Transforming Growth Factor ◽  
Oral Submucous Fibrosis ◽  
Transforming Growth Factor Β ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Research Progress ◽  
Areca Nut ◽  
Related Factors ◽  
Oral Potentially Malignant Disorders ◽  
Submucous Fibrosis

Oral Submucous Fibrosis (OSMF) is an oral mucosal disease with lamina propria collagen hyperplasia as the main pathological change, which belongs to Oral Potentially Malignant Disorders (OPMDs). Areca nut is identified as a class I carcinogen with complex components. Arecoline is the main component of areca nut which plays an important role in the pathogenesis of OSMF. Through the review of literature, it is shown that arecoline can lead to the change in level of cytokines in oral mucosa, which further leads to the imbalance of collagen metabolism. This article reviews the molecular mechanism research progress of arecoline in promoting the pathogenesis of OSMF in recent years, including Transforming Growth Factor-β (TGF-β) and Reactive Oxygen Species (ROS) associated with increased collagen production, Matrix Metalloproteinase (MMP) and Tissue Inhibitor of Metalloproteinase (TIMP) associated with reduced collagen degradation, hypoxia and microvascular related factors and in order to provide reference for the treatment of the disease at the molecular level.

Perianale Fisteln bei CED: vom Mausmodell zur Klinik

2018 ◽  
Vol 75 (5) ◽  
pp. 287-294
Author(s):  
Michael Scharl
Keyword(s):  
Growth Factor ◽  
Morbus Crohn ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 13

Zusammenfassung. Fisteln stellen nach wie vor eine der wichtigsten Komplikationen bei Patienten mit Morbus Crohn dar. Bei mindestens einem Drittel aller Morbus Crohn Patienten treten im Laufe der Erkrankung Fisteln auf. Eine dauerhafte Heilung der Fistel wird jedoch, auch unter Ausschöpfung sämtlicher medikamentöser und chirurgischer Therapieoptionen, nur in rund einem Drittel dieser Patienten erreicht. Der genaue molekulare Mechanismus der Fistelentstehung ist bis heute nicht ganz klar. Aus histopathologischer Sichtweise stellen Fisteln eine röhrenartige Struktur dar, welche von flachen epithelartigen Zellen ausgekleidet ist. Als ursächlicher Entstehungsmechanismus wird dabei die sogenannte epitheliale-zu-mesenchymale Transition (EMT) angesehen und es kann eine starke Expression der Entzündungsmediatoren Tumor Nekrose Faktor, Interleukin-13 und Transforming Growth Factor β in den Fistelarealen nachgewiesen werden. Zusätzlich zu den bereits etablierten, medikamentösen Therapieoptionen, also Antibiotika, Immunmodulatoren und anti-TNF Antikörper, stellt insbesondere der Einsatz der mesenchymalen Stammzelltherapie einen erfolgversprechenden Therapieansatz für die Zukunft dar.

A Novel Missense Mutation in the Endoglin Gene in Hereditary Hemorrhagic Telangiectasia

1997 ◽  
Vol 77 (02) ◽  
pp. 243-247 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Hiroyuki Azuma ◽  
Toshio Shigekiyo ◽  
Hideo Inoue ◽  
Shiro Saito
Keyword(s):  
Missense Mutation ◽  
Hereditary Hemorrhagic Telangiectasia ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Autosomal Dominant Disorder ◽  
Her Family ◽  
Normal Individuals ◽  
Oligonucleotide Hybridization ◽  
Vascular Dysplasia ◽  
Exon 4

SummaryHereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by multisystem vascular dysplasia and recurrent hemorrhage. Recent investigation has mapped one of the responsible genes for HHT to chromosome 9q33-q34; subsequently, nine different mutations have been identified in the endoglin gene, which encodes a transforming growth factor β(TGF-β) binding protein, in nine unrelated families with HHT. We examined the endoglin gene in a Japanese patient with HHT and her family members. Using PCR-SSCP. analysis followed by sequencing, we identified a C to A missense mutation in exon 4 which changed an Ala160 codon(GCT) to an Asp160 codon (GAT). Since this mutation destroys one of three Fnu4H I sites in exon 4, the Fnu4H I digestion patterns of the PCR-amplified exon 4 fragments from each family member were analyzed. In affected members, the restriction patterns were all consistent with a phenotype of HHT. PCR-amplified exon 4 fragments from 150 normal individuals were also analyzed by allele-specific oligonucleotide hybridization analysis. As a result, the mutation was not found in any of them. We conclude that the C to A mutation in exon 4 of the endoglin gene in this proband is responsible for the occurrence of HHT in this family.

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