The most abundant cell type in lung interstitium is fibroblasts. They resemble ordinary fibroblasts but have some distinguishing features, such as long branching processes and gap junctions. HPF main function is to produce type III collagen, elastin, and proteoglycans of the extracellular matrix of the alveolar septa. Pulmonary fibroblasts (PF) play an important role in the repair and remodeling processes following injury. The controlled accumulation of fibroblasts to sites of inflammation is crucial to effective tissue repair after injury. Either inadequate or excessive accumulation of fibroblasts could result in abnormal tissue function. For example, the excess proliferation of fibroblasts contributes to the adventitial thickening observed during the development of hypoxia-induced pulmonary hypertension.
HPF-a from ScienCell Research Laboratories are isolated from adult human lung tissue. HPF-a are cryopreserved at passage one and delivered frozen. Each vial contains >5 x 105 cells in 1 ml volume. HPF-a are characterized by immunofluorescence with antibody specific to fibronectin. HPF-a are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi. HPF-a are guaranteed to further expand for 15 population doublings under the conditions provided by ScienCell Research Laboratories.
Recommended Medium
It is recommended to use Fibroblast Medium (FM, Cat. #2301) for the culturing of HPF-a in vitro.
成纤维细胞是肺间质中最丰富的细胞类型。它们与普通成纤维细胞形态相似，但具有一些独特特征，例如细长的分支状突起和缝隙连接。人肺成纤维细胞（HPF）的主要功能是合成肺泡隔细胞外基质中的Ⅲ型胶原蛋白、弹性蛋白和蛋白聚糖。肺成纤维细胞（PF）在肺组织损伤后的修复和重塑过程中发挥重要作用。损伤发生后，成纤维细胞受调控地聚集于炎症部位，对于有效的组织修复至关重要。成纤维细胞聚集不足或过度聚集均可能导致组织功能异常。例如，成纤维细胞过度增殖会促进肺动脉外膜增厚，这是缺氧诱导的肺动脉高压发生发展过程中常见的病理变化。
ScienCell Research Laboratories 的人肺成纤维细胞（成人）（HPF-a）分离自人成人肺组织。HPF-a 以第 1 代（P1）冻存，并以冷冻状态运输。每瓶含有 >5 × 105 个细胞，体积为 1 ml。HPF-a 采用针对纤连蛋白（fibronectin）的特异性抗体进行免疫荧光鉴定。HPF-a 经检测对 HIV-1、HBV、HCV、支原体、细菌、酵母菌和真菌均呈阴性。在 ScienCell Research Laboratories 提供的培养条件下，HPF-a 可进一步扩增 15 个群体倍增（population doublings）。
推荐培养基
推荐使用成纤维细胞培养基（Fibroblast Medium，FM，产品编号：2301）在体外培养 HPF-a。
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Due to tumor heterogeneity, most believe that effective treatments should be tailored to the features of an individual tumor or tumor subclass. It is still unclear, howev... More
Due to tumor heterogeneity, most believe that effective treatments should be tailored to the features of an individual tumor or tumor subclass. It is still unclear, however, what information should be considered for optimal disease stratification, and most prior work focuses on tumor genomics. Here, we focus on the tumor microenvironment. Using a large‐scale coculture assay optimized to measure drug‐induced cell death, we identify tumor–stroma interactions that modulate drug sensitivity. Our data show that the chemo‐insensitivity typically associated with aggressive subtypes of breast cancer is not observed if these cells are grown in 2D or 3D monoculture, but is manifested when these cells are cocultured with stromal cells, such as fibroblasts. Furthermore, we find that fibroblasts influence drug responses in two distinct and divergent manners, associated with the tissue from which the fibroblasts were harvested. These divergent phenotypes occur regardless of the drug tested and result from modulation of apoptotic priming within tumor cells. Our study highlights unexpected diversity in tumor–stroma interactions, and we reveal new principles that dictate how fibroblasts alter tumor drug responses. Less
Autophagy, a type II programmed cell death, is essential for cell survival under stress, e.g. lung injury, and bone marrow-derived mesenchymal stem cells (BM-MSCs) have g... More
Autophagy, a type II programmed cell death, is essential for cell survival under stress, e.g. lung injury, and bone marrow-derived mesenchymal stem cells (BM-MSCs) have great potential for cell therapy. However, the mechanisms underlying the BM-MSC activation of autophagy to provide a therapeutic effect in ischaemia/reperfusion-induced lung injury (IRI) remain unclear. Thus, we investigate the activation of autophagy in IRI following transplantation with BM-MSCs. Seventy mice were pre-treated with BM-MSCs before they underwent lung IRI surgery in vivo. Human pulmonary micro-vascular endothelial cells (HPMVECs) were pre-conditioned with BM-MSCs by oxygen-glucose deprivation/reoxygenation (OGD) in vitro. Expression markers for autophagy and the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signalling pathway were analysed. In IRI-treated mice, administration of BM-MSCs significantly attenuated lung injury and inflammation, and increased the level of autophagy. In OGD-treated HPMVECs, co-culture with BM-MSCs attenuated endothelial permeability by decreasing the level of cell death and enhanced autophagic activation. Moreover, administration of BM-MSCs decreased the level of PI3K class I and p-Akt while the expression of PI3K class III was increased. Finally, BM-MSCs-induced autophagic activity was prevented using the inhibitor LY294002. Administration of BM-MSCs attenuated lung injury by improving the autophagy level via the PI3K/Akt signalling pathway. These findings provide further understanding of the mechanisms related to BM-MSCs and will help to develop new cell-based therapeutic strategies in lung injury. Less
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