In re-cent 20 years, the development of cell biology technology has promoted the research of keloid. Keloid fibroblasts (KFbs) are the main effector cells in keloid, which are closely related to the occurrence and development of keloid. It is significantly different in terms of biological characteristics and gene expression between KFbs and normal fibroblasts. This articles reviews the characteristics of KFbs from multiple perspectives, describing its biological character- istics in details including microstructures, metabolic character- istics, and proliferation properties, and introducing the main characteristics of heterogeneity and genomics of KFbs. The further research on KFbs will help to elucidate the pathogenesis of keloids and provide valuable strategies for the prevention and treatment of keloids.
Fibroblasts/metabolism* ; Humans ; Keloid/pathology*

Coronary Restenosis ; pathology ; Fibroblasts ; metabolism ; pathology ; Fibrosis

Cancer-associated fibroblasts （CAF） are a key component of the tumor microenvironment, which can secrete a variety of cytokines, chemokines and growth factors, directly and indirectly support cancer cells, also alter the immune cellular environment by inhibiting the activity of immune effector cells and recruiting immunosuppressive cells, thereby allowing cancer cells to evade immune surveillance. CAF has been proven to be associated with the development, progression, and poor prognosis of solid tumors. However, the role of CAF in hematological malignancies is still unclear. This article reviews the research progress of CAF in hematological malignancies.
Humans ; Cancer-Associated Fibroblasts/pathology* ; Neoplasms/metabolism* ; Hematologic Neoplasms/metabolism* ; Tumor Microenvironment ; Fibroblasts/pathology*

Hypertrophic scar is a pathological repair result of excessive accumulation of extracellular matrix after skin damage, which affects the appearance and function of patients with varying degrees. The degree of scar formation is directly related to the strength of inflammatory reaction during wound healing, and excessive or prolonged inflammatory response increases the incidence of hypertrophic scars. Interleukin-6 (IL-6) is a pleiotropic cytokine that is involved in regulating the fibrotic network composed of fibroblasts, macrophages, keratinocytes, and vascular endothelial cells, and is closely related to the formation of hypertrophic scars. This article reviews the role of IL-6 and its signaling pathway in hypertrophic scar formation.
Cicatrix, Hypertrophic/pathology* ; Endothelial Cells/metabolism* ; Fibroblasts/metabolism* ; Humans ; Interleukin-6 ; Skin/pathology* ; Wound Healing/physiology*

OBJECTIVETo study the expression of P57(kip2) and Maspin in the pathological scar and their possible role in the pathogenesis of abnormal scars.

METHODSImmunohistochemistry integrated image analysis and reverse transcription polymerase chain reaction (RT-RCR) were performed to detect the expression of P57(kip2) and Maspin in hypertrophic scar, keloid, mature scar and normal skin. Statistics was used to analyze the datas.

RESULTSThe expression of P57(kip2) protein was fixed to fibroblast intranuclear in abnormal scar, and the expression of P57(kip2) protein and P57(kip2) mRNA decreased (P < 0.05). The expression of Maspin protein was fixed to fibroblast cytoplasm and intranuclear in abnormal scar, and the expression of Maspin protein and Maspin mRNA decrease, compared with that in normal group (P < 0.05). There was positive correlation between P57(kip2) protein and Maspin protein expression (P < 0.01).

CONCLUSIONSThe decreased expression of P57(kip2) and Maspin in abnormal scar shows that they are cicatrix-related genes. There is a positive relationship between the two genes. It may be one of the mechanisms of pathogenesis of abnormal scar. It makes effect through fibroblasts.

Cicatrix ; metabolism ; pathology ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Cyclin-Dependent Kinase Inhibitor p57 ; metabolism ; Fibroblasts ; metabolism ; Humans ; Serpins ; metabolism

OBJECTIVETo investigate the role of lung fibroblast activation in radiation-induced lung injury.

METHODSThirty-five male Wistar rats were exposed to a single-dose 30 Gy irradiation of the right hemithorax or sham right lung irradiation. At 1, 7, 14, 28, 56 or 84 days after the irradiation, the rats were sacrificed for examination of alpha-smooth muscle actin (alpha-SMA) expression in the bilateral lung tissues using immunohistochemistry.

RESULTSalpha-SMA expression in fibroblast increased significantly in the out-field and in-field lung tissues within 24 h after irradiation after the irradiation (P<0.001).

CONCLUSIONActivation of the lung fibroblasts occurred within 24 h after irradiation and found in ont-field and in-field lung tissues, suggesting that radiation-induced lung injury may not have an obvious latency.

Actins ; genetics ; metabolism ; Animals ; Fibroblasts ; metabolism ; pathology ; Lung ; cytology ; pathology ; Male ; Radiation Injuries ; pathology ; Rats ; Rats, Wistar

The objective of this study was to investigate the effect of cytomegalovirus (CMV) infection on actin and microfilament in human embryo fibroblast cells (HF) and to explore the possible relationship with CMV replication. The cell shape was observed by microscopy after the infection of CMV, RT-PCR assay was used to detect the mRNA expression of beta-actin gene, while Westen-blot was used to measure the level of beta-actin protein. CMV immediately early antigen (IE) in HF cells was analyzed by indirect immunofluorescence assay. Microfilament alteration was determined by cytoskeleton fluorescence probe. The results showed that CMV IE was observed in more than 95% of HF cells after infection, primarily located in nucleus. HF cells infected by CMV changed from thin shuttle shape to round and thick ball shape, even detached from wall. Beta-actin got a significant and gradual decreasing of mRNA level in time-dependent manner (P < 0.05). Compared with uninfected group, the expression of beta-actin protein decreased to (74.2 +/- 13.4)% at 96 hours after infection (P < 0.05). In infected HF cells, microfilaments were ruptured, arranged turbulently, as well as cells merged and fluorescence density of microfilament obviously reduced. It is concluded that cytomegalovirus can induce alteration of actin and microfilament, which may be helpful for CMV to infect, replicate and reactivate in host cells.
Actin Cytoskeleton ; metabolism ; ultrastructure ; Actins ; metabolism ; Cell Line ; Cytomegalovirus Infections ; metabolism ; pathology ; Fibroblasts ; pathology ; ultrastructure ; virology ; Humans

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease caused by inflammatory cells. Various inflammatory cells involved in RA include fibroblast-like synoviocytes, macrophages, CD4⁺T-lymphocytes, B lymphocytes, osteoclasts and chondrocytes. The close interaction between various inflammatory cells leads to imbalance of immune response and disorder of the expression of mRNA in inflammatory cells. It helps to drive production of pro-inflammatory cytokines and stimulate specific antigen-specific T- and B-lymphocytes to produce autoantibodies which is an important pathogenic factor for RA. Competing endogenous RNA (ceRNA) can regulate the expression of mRNA by competitively binding to miRNA. The related ceRNA network is a new regulatory mechanism for RNA interaction. It has been found to be involved in the regulation of abnormal biological processes such as proliferation, apoptosis, invasion and release of inflammatory factors of RA inflammatory cells. Understanding the ceRNA network in 6 kinds of RA common inflammatory cells provides a new idea for further elucidating the pathogenesis of RA, and provides a theoretical basis for the discovery of new biomarkers and effective therapeutic targets.
Humans ; Arthritis, Rheumatoid/genetics* ; MicroRNAs/metabolism* ; Synoviocytes/pathology* ; Cytokines/metabolism* ; RNA, Messenger/metabolism* ; Fibroblasts/pathology* ; Cell Proliferation

Epithelial-mesenchymal transition (EMT) is a process by which fully differentiated epithelial cells undergo a phenotypic conversion and assume a mesenchymal cell phenotype, including elongated morphology, enhanced migratory and invasiveness capacity, and greatly increased production of extracellular matrix (ECM) components. The EMTs associated with wound healing, tissue regeneration, and organ fibrosis are termed as type 2 EMT. Over the past two decades, emerging evidence suggested that injured epithelial cells, via type 2 EMT, may serve as important sources of fibroblasts and contribute to organ fibrosis, such as kidney, liver, lung and eyes. There is perhaps no doubt that adult epithelial cells can undergo EMT in vitro in response to transforming growth factor (TGF)-β1 and other inflammatory or pro-fibrotic stimuli. However, whether type 2 EMT really occurs in vivo, whethers it is actually a source of functional and activated interstitial fibroblasts and whether it contributes to tissue fibrosis have already been the subjects of heated debate. In this review, we will describe the main features of EMT, the major findings of type 2 EMT in vitro, the evidences for and against type 2 EMT in vivo and discuss the heterogeneity and pitfalls of the techniques used to detect EMT during fibrotic diseases. We suggest that in order to ascertain the existence of type 2 EMT in vivo, different proper phenotype markers of epithelial and mesenchymal cells should be jointly used and cell lineage tracking techniques should be standardized and avoid false positives. Finally, we believe that if EMT really occurs and contributes to tissue fibrosis, efforts should be made to block or reverse EMT to attenuate fibrotic process.
Animals ; Epithelial-Mesenchymal Transition ; physiology ; Fibroblasts ; cytology ; metabolism ; Fibrosis ; metabolism ; pathology ; Humans

Animals ; Arthritis, Experimental ; metabolism ; pathology ; Breast Neoplasms ; pathology ; Cadherins ; metabolism ; physiology ; Cell Movement ; Female ; Fibroblasts ; cytology ; pathology ; Humans ; Macrophages ; cytology ; pathology ; Neoplasm Invasiveness ; Synovial Membrane ; cytology ; metabolism ; pathology