Objective To compare the differences of chromosome aberration and Rb 1 gene mutation among 3 cloned cells of SO-Rb50 cell line of retinoblastoma. Methods 1.Three cell cloned strains named MC2, MC3, MC4 were isolated from SO-Rb50. 2. Gbanding and karyotype analysis were performed on the llth passage cells of the 3 cell strains.3.All exons and the promoter region of the Rb gene were detected by PCR-SSCP analysis in tumor cell DNA extracted from the 3 cell strains. Results 1.Both numerical and structural chromosomal aberrations could be observed in these 3 cell strains.Several kinds of structural chromosomal aberrations were observed.The chromosome aberrations in the same passage of different cell strains were different.Aberration of chromosome 13 was rare and the aberration feature was different in the 3 cell strains.Five marker chromosomes were identified.M1,t(1;1)qter-p35∷q24-ter could befound in all cell strains.Two of them M4 and M5,have not been reported in SO-Rb50 cell line previously.2.SSCP analysis of exon 24 showed that MC411 and MC3138 had abnormal band. Conclusions The characteristics of heterogeneity of the original tumor cell line SO-Rb50are still kept during a long-term culture in vitro and the cloned strains had dynamic changes during this period.Aberration of chromosome 13 is not the only cause of RB;aberration of chromosome 1,a commom event in some neoplasias as well as in SO-Rb50, plays a meaningful role in the immortalization of this cell line. (Chin J Ocul Fundus Dis, 1999, 15: 146-148)
ObjectiveTo review the research advances in molecular biology of vascular restenosis.MethodsThe literatures about molecular biology of vascular restenosis were reviewed.ResultsCurrent transgenic ways had some advantages and disadvantages. Gene therapy with HSV-tk, Rb,p21，p27,p53,c-myc, c-myb, vascular endothelial growth factor,bFGF,platelet derived growth facfor，nuclear factor-κB and so on inhibited vascular restenosis.ConclusionA better transgenic system and gene-combination therapy will be effective to treat vascular restenosis.
ObjectiveTo understand the progress of molecular biology research on the pathogenesis of hemorrhoids. MethodThe literatures relevant to reseaches on the molecular biology of hemorrhoid pathogenesis in recent years had been reviewed. ResultsThe generally accepted theories of hemorrhoids included anal cushion downward movement theory, varicose vein theory, and vascular proliferation theory. The molecular biological studies related to the theory of anal cushion downward movement found that the increased expression of matrix metalloproteinase-9 and the abnormal expression of smooth muscle actin could damage the supporting tissue of anal cushion, causing the downward movement and prolapse of anal cushion, and then formed hemorrhoids; The molecular biology researches related to varicose vein theory found that the increase of nitric oxide synthase and transient receptor potential vanilloid 1 could promote the production of nitric oxide, causing varicose veins, and then leaded to the pathogenesis of hemorrhoids; The molecular biology researches related to vascular proliferation theory found that the low expressions of miR-412-5p and miR-4729, and the overexpressions of vascular endothelial growth factor and fibroblast growth factor were related to the vascular proliferation of hemorrhoids. In addition, the secondary inflammatory reaction after the onset of hemorrhoids also played an important role in the occurrence and development of hemorrhoids. ConclusionsThe occurrence and development of hemorrhoids is the result of the intersection and interaction of various mechanisms such as anal cushion downward movement, varicose veins, vascular proliferation, and secondary inflammatory reaction. The molecular biology research on the pathogenesis of hemorrhoids is helpful to better explain the occurrence of hemorrhoids from a microcosmic perspective, and lay a foundation for further exploring the etiology of hemorrhoids.
Objective To review the research progress of pathological changes of glenohumeral capsule in patients with recurrent shoulder anterior dislocation (RSAD). Methods The literature on shoulder capsules, both domestic and international, was reviewed. The anatomy, histology, and molecular biology characteristics of the glenohumeral capsule in RSAD patients were summarized. Results Anatomically, the glenohumeral capsule is composed of four distinct parts: the upper, lower, anterior, and posterior sections. The thickness of these sections is uneven, and the stability of the capsule is further enhanced by the presence of the glenohumeral and coracohumeral ligaments. Histologically, the capsule tissue undergoes adaptive changes following RSAD, which improve its ability to withstand stretching and deformation. In the realm of molecular biology, genes associated with the regulation of structure formation, function, and extracellular matrix homeostasis of the shoulder capsule’s collagen fibers exhibit varying degrees of expression changes. Specifically, the up-regulation of transforming growth factor β1 (TGF-β1), TGF-β receptor 1, lysyl oxidase, and procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 facilitates the repair of the joint capsule, thereby contributing to the maintenance of shoulder joint stability. Conversely, the up-regulation of collagen type Ⅰ alpha 1 (COL1A1), COL3A1, and COL5A1 is linked to the recurrence of shoulder anterior dislocation, as these changes reflect the joint capsule’s response to dislocation. Additionally, the expressions of tenascin C and fibronectin 1 may play a role in the pathological processes occurring during the early stages of RSAD. ConclusionGlenohumeral capsular laxity is both a consequence of RSAD and a significant factor contributing to its recurrence. While numerous studies have documented alterations in the shoulder capsule following RSAD, further research is necessary to confirm the specific pathological anatomy, histological, and molecular biological changes involved.
Objective The currently pertinent articles about the molecular mechanism of recurrence and metastasis of primary hepatocellular carcinoma (HCC) were reviewed. Methods Literatures that related to the molecular mechanism of the recurrence and metastasis of HCC were summarized retrospectively in this review. Results Several genes, such as the growth factors and the corresponding receptors, the adhesive molecule, and the extracellular matrix and many factors, such as the oxygen supply, tumor angiogenesis and the immune system, all took important roles in the process of recurrence and metastasis of HCC, which involves many steps. Conclusion The study of the recurrence and metastasis of HCC should be emphasized further since early intervening the genes that are related to the recurrence and metastasis may help prevent the recurrence and metastasis of HCC completely, decrease the death rate and improve patients’ life quality in the long term.
Objective To summarize the molecular biological research progress of non-coding RNAs modulating osteoarthritis (OA), and provide a reference basis for biological study and clinical treatment of OA. Methods Recent domestic and foreign related literature about the regulation of OA pathological process by non-coding RNAs was widely reviewed. Results Non-coding RNAs can be divided into three types based on the length of RNA. A lot of non-coding RNAs participating in OA pathological process are screened out by high throughput sequencing technology and microarray technology, and it is verified that these non-coding RNAs involve in the regulation of OA by RT-PCR. The mechanism of OA mediated target is clarified by knocking-down and overexpressing of the most prominent expressed non-coding RNAs in OA. There are the complicated gene expressed network topology in non-coding RNAs, and between non-coding RNAs and coding RNAs. It provides a basis for clearing the effect of gene structure and function, and finding the definite therapeutic target of OA. Conclusion There is preliminary study on molecular biological mechanism of non-coding RNAs mediating OA, but the key structure or sequence of non-coding RNAs, formation and interaction of effecting composite structure about mediating OA are unknown, and it needs further study.