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At least 19 recordsLinked to original sources
PubMed2026

Complement expression profiles in human glomerular mesangial cells, endothelial cells, podocytes and proximal tubular epithelial cells.

BACKGROUND: Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue. METHODS: Complement expression in cultured human renal intrinsic cells was initially evaluated using reverse transcription polymerase chain reaction and immunofluorescence staining. These findings were further examined using publicly available single-cell RNA-sequencing datasets and 10×Genomics single-cell RNA sequencing of non-diseased human kidney tissue. The analyses focused on complement components involved in the initiation of the classical, lectin, and alternative pathways, as well as components shared among these activation pathways, terminal pathway components, complement regulators, and complement receptors. RESULTS: Complement components unique to the initial phase for classical pathway (C1S, C1R, C2, C4), lectin pathway (MBL2, FCN1, MASP1), alternative pathway (CFB, CFD), and the C3 component shared by the three activation pathways were detected in these cells. The components shared by the terminal pathways including C5, C6, C7, C8 and C9 exhibited lower expression, while complement regulators (CFH, CFI, CD55/DAF, CD46/MCP, CD59, C4BPB, PROS1/Protein S) or receptors (CD93/C1QR1, CR1), particularly membrane-bound proteins, such as DAF, MCP and CD59, which inhibit complement activation and the formation of the membrane attack complex, showed relatively high expression. CONCLUSION: These results showed that all four types of intrinsic renal cells expressed multiple complement components associated with the classical, lectin, and alternative pathways. In non-diseased kidney tissue, complement regulatory molecules involved in the control of complement activation showed relatively higher expression, whereas components of the terminal complement pathway were expressed at relatively lower levels, suggesting that renal intrinsic cells maintain a locally poised but tightly regulated complement system.

Humans↗
PubMed1977

Production of 5-hydroxyindoleacetic acid from serotonin by cultured endothelial cells.

Endothelial cells cells from bovine aorta and human umbilical vein and fibroblasts from human foreskin were cultured and subsequently evaluated for ability to metabolize serotonin (5-HT) to 5-hydroxyindoleacetic acid (5-HIAA). Cells were incubated for three hours with 4 X 10(-6) M [14C] 5-HT creatinine sulfate. [14C] 5-HIAA was separated from labeled 5-HT by column chromatography and measured for scintillation counting. Production of 5-HIAA by bovine aorta cells was 39.0+/-7.5 (S.E.M., n=6) nmoles per 10(9) cells per hour. Production of 5-HIAA was markedly inhibited by the presence of 10(-4) M iproniazid (an inhibitor of monoamine oxidase) or 10(-4) M imipramine (an inhibitor of amine transport). 5-HIAA was the only product of 5-HT metabolism detected by thin layer chromatography. Production of 5-HIAA by human umbilical vein endothelial cells was 5.4+/-2.0 nmoles per 10(9) cells per hour (n=5) and by human foreskin fibroblasts was 3.9+/-1.4 nmoles per 10(9) cells per hour (n=5). The results obtained during incubation in the presence and absence of inhibitors indicate that bovine aorta endothelial cells maintained in tissue culture are able to transport serotonin with subsequent production of 5-HIAA. By contrast, human umbilical vein endothelial cells and fibroblasts exhibited relatively low rates of 5-HT uptake and metabolism.

Animals↗
PubMed1979

Purine metabolism in cultured coronary endothelial cells.

Endothelial cells from coronary vessels of guinea pig hearts were isolated, cultivated and morphologically characterized. --Cells from confluent cultures contained adenine nucleotides and their dephosphorylated degradatives in exceptionally high amounts. --Adenine nucleotide levels were only slightly influenced by the growth state of the cultures and remained stable during incubation for three days in purine-free medium. In contrast, brief incubation of endothelial cells under anoxic conditions resulted in a substantial breakdown of adenine nucleotides associated with an enhanced formation and release of adenosine. --Measurements of specific activities of enzymes involved in adenine nucleotide synthesis and degradation lend additional support to the view that a very active adenine nucleotide metabolism is a typical feature of cultured coronary endothelial cells.

Adenine Nucleotides↗
PubMed1975

Synthesis of factor VIII antigen by cultured human endothelial cells.

Endothelial cells have been isolated from freshly obtained human umbilical cords by collagenase digestion of the interior of the umbilical vein and grown in tissue culture. These cells have been identified by morphologic and immunologic criteria. It has been demonstrated that these cultured human endothelial cells synthesize and release factor VIII antigen but not factor VIII clot-promoting activity.

Animals↗
PubMed1975

Immunological studies of human placentae. Binding of complexed immunoglobulin by stromal endothelial cells.

Endothelial cells of foetal stem vessels in cryostat sections of normal, full-term human placentae bind fluorescein-conjugated heat-aggregated human IgG. Soluble immune complexes of sheep anti-human albumin also bind in a pattern that is similar to that of aggregated human IgG, but native human IgG is not bound by placental endothelial cells. Aggregated IgG binding, unlike soluble immune complexes, is blocked by pretreatment of the sections with antiserum to human IgM. Cross-blocking experiments with aggregated IgG and immune complexes suggest that they may be bound by different receptors.

Antigen-Antibody Complex↗
PubMed1975

Proliferation of mononuclear phagocytes (Kupffer cells) and endothelial cells in regenerating rat liver. A light and electron microscopic cytochemical study.

The proliferation of littoral cells in regenerating rat liver after partial hepatectomy has been investigated using endogenous peroxidase and uptake of large (0.8-mu) latex particles as markers of Kupffer cells. Female rats were subjected to 2/3 partial hepatectomy and sacrificed at intervals up to 11 days. Prior to sacrifice, animals were injected with latex and their livers were fixed by perfusion and were processed for cytochemical localization of peroxidase. The sinusoidal cells exhibited a marked regenerative response after partial hepatectomy. Peroxidase activity persisted in endoplasmic reticulum of Kupffer cells during mitosis. Furthermore, latex particles were exclusively localized in such peroxidase-positive cells, thus confirming their identity as Kupffer cells. Quantitative counts revealed that the peak mitotic activity of Kupffer cells occurred at 48 hours, whereas that of endothelial cells was at 96 hours after partial hepatectomy. Our findings indicate that Kupffer cells are capable of dividing locally in the liver; no morphologic evidence of transformation of endothelial cells or monocytes to Kupffer cells was found. The significance of these observations concerning the origin of Kupffer cells is discussed, and it is concluded that in the model of liver regeneration after partial hepatectomy the Kupffer cells are formed predominantly by local cell division.

Animals↗
PubMed1978

Desmosome-like structures between tumor cells and endothelial cells in choriocarcinoma heterotransplanted into the nude mouse: a preliminary report.

Tumor cells obtained from the metastatic focus of the lung of a 51-year-old woman with choriocarcinoma were transplanted in the subcutaneous tissue of the nude mouse and studied with an electron microscope. At the junctional zone between the tumor and the invaded cells a desmosome-like structure, between the transplanted tumor cells and endothelial cells, was observed in the nude mouse. Although this finding seems quite unusual, it may be related to the unique character of the early trophoblast.

Animals↗
PubMed1978

Effects of glucocorticoids on the interaction of lymphoblastoid cells with human endothelial cells in vitro.

The adhesive characteristics of cultured acute lymphocytic leukemia cells (CCRF-CEM), lymphoma cells (Raji), and freshly isolated acute lymphocytic leukemia cells to human cultured endothelial cells were studied. An assay system was used whereby these neoplastic cells were allowed to interact with endothelial cells while being continuously agitated on a rocking platform. All cell lines adhered significantly to the endothelium monolayers. This process appeared not to be dependent upon intact microtubular or microfilament function. Likewise, removing surface sialic acid from either cell type did not alter this process. In contrast incubating the endothelial cells for 24 or 48 hr with dexamethasone decreased adhesiveness of either CCRF-CEM or Raji cells to the endothelial cells by approximately 40%. Incubating these cells with hydrocortisone instead of dexamethasone for 48 hr was equally as effective in altering the endothelial cell adhesiveness. The decreased adhesiveness could be blocked by cycloheximide, indicating that this altered adhesiveness of the endothelial cells involves protein synthesis, presumably of a surface protein. We suggest that this assay system may provide a means to evaluate other agents that can alter the surface characteristics of endothelial cells, which may have important implications in various disease states such as inflammation, thrombogenesis, and metastatic disease.

Blood Vessels↗
PubMed1979

Interactions of tumor cells with vascular endothelial cell monolayers: a model for metastatic invasion.

The interactions of tumorigenic and nontumorigenic human and rodent cells with vascular endothelial cells and their underlying extracellular matrix were studied in culture. The abilities of various cells to attach to endothelial monolayers and cause morphologic changes, such as rupture of endothelial-endothelial cell interactions leading to retraction of endothelial cells and exposure of extracellular matrix, as well as their propensities to invade and underlap retracted endothelial monolayers and continue migration were assessed by time-lapse and phase-contrast microscopy as well as scanning and transmission electron microscopy. In general, highly malignant or highly invasive cells in vivo were capable of attachment, invasion, and migration under endothelial cells in vitro. This system may be useful for elucidating mechanisms of tumor cell arrest and extravasation.

Animals↗
PubMed1979

Long-term culture of capillary endothelial cells.

Capillary endothelial cells from rats, calves, and humans, have been carried in long-term culture. Bovine capillary endothelial cells have been cloned and maintained by serial passage for longer than 8 months. This prolonged culture was accomplished by using tumor-conditioned medium, gelatin-coated plates, and a method of enriching cells in primary culture. Cultured bovine capillary endothelial cells produce Factor VIII antigen and angiotensin-converting enzyme, but do not have Weibel-Palade bodies. Human cells do contain Weibel-Palade bodies. Capillary endothelial cells are distinguished from aortic endothelial cells by their requirement for conditioned medium. Bovine capillary endothelial cells in regular medium grow slowly with a mean doubling time of 67 hr and eventually die. In tumor-conditioned medium, these cells grow rapidly with a doubling time of 28 hr and continue to proliferate for as long as the tumor-conditioned medium is present. In contrast, bovine aortic endothelial cells grow as rapidly in regular medium as in tumor-conditioned medium. This method allows the production of pure capillary endothelial cells that may prove useful for studies of tumor angiogenesis, metastatic mechanisms, and the role of capillary endothelium in other pathologic states.

Adrenal Glands↗
PubMed1975

The identification of HL-A antigens on fresh and cultured human endothelial cells.

Human endothelial cells were obtained from the umbilical cord veins of 16 newborns by methods previously described and tested for HL-A antigens by a microcytotoxicity method. HL-A antigens were present on all endothelial cell lines tested. When the HL-A phenotypes of fresh endothelial cells and autologous fetal lymphocytes were compared, a concordance of 70% was observed. When the HL-A phenotypes of maternal lymphocytes and fresh endothelial cells were compared, a maternal contribution to the endothelial cell phenotype was evident in 72% of the possible commmon antigens. Some HL-A antigens were deleted from 11 of 16 endothelial cell lines that were re-typed after 2 weeks in tissue culture. The majority (90%) of deleted antigens were from the second HL-A locus. When three lines of endothelials cells were again re-typed after 6 weeks in culture, no further changes in antigenicity were noted. These findings: a) demonstrate that HL-A antigens are present on human endothelium and suggest that endothelial cells are actively involved in establishing the immunogenicity of a graft, and b) demonstrate that the HL-A antigens on human endothelial cells may be modulated by in vitro culture.

Adult↗
PubMed1978

Control of proliferation of human vascular endothelial cells. Characterization of the response of human umbilical vein endothelial cells to fibroblast growth factor, epidermal growth factor, and thrombin.

Because the response of human endothelial cells to growth factors and conditioning agents has broad implications for our understanding of wound healing angiogenesis, and human atherogenesis, we have investigated the responses of these cells to the fibroblast (FGF) and epidermal growth factors (EGF), as well as to the protease thrombin, which has been previously shown to potentiate the growth response of other cell types of FGF and EGF. Because the vascular endothelial cells that form the inner lining of blood vessels may be expected to be exposed to high thrombin concentrations after trauma or in pathological states associated with thrombosis, they are of particular interest with respect to the physiological role of this protease in potentiating cell proliferation. Our results indicate that human vascular endothelial cells respond poorly to either FGF or thrombin alone. In contrast, when cells are maintained in the presence of thrombin, their proliferative response to FGF is greatly increased even in cultures seeded at a density as low as 3 cells/mm2. Human vascular endothelial cells also respond to EGF and thrombin, although their rate of proliferation is much slower than when maintained with FGF and thrombin. In contrast, bovine vascular endothelial cells derived from vascular territories as diverse as the bovine heart, aortic arch, and umbilical vein respond maximally to FGF alone and neither respond to nor bind EGF. Furthermore, the response of bovine vascular endothelial cells to FGF was not potentiated by thrombin, indicating that the set of factors controlling the proliferation of vascular endothelial cells could be species-dependent. The requirement of cultured human vascular endothelial cells for thrombin could explain why the human cells, in contrast to bovine endothelial cells, are so difficult to maintain in tissue culture. Our results demonstrate that by using FGF and thrombin one can develop cultures of human vascular endothelial cells capable of being passage repeatedly while maintaining a high mitotic index. The stock cultures used for these studies have been passed weekly with a split ratio of 1 to 10 and are currently in their 30th passage. These cultures are indistinguishable from earlier passages when examined for the presence of Weibel-Palade bodies or Factor VIII antigen. We conclude that the use of FGF and thrombin can prevent the precocious senescence observed in most human endothelial cells cultures previously described.

Animals↗
PubMed1975

Culture of arterial endothelial cells: characterization and growth of bovine aortic cells.

Arterial endothelial cells were obtained from bovine aortae by mild treatment with collagenase and medium perfusion. These cells were cultured in RPMI-1640 medium containing 15mM Hepes buffer and 35% fetal calf serum at pH 7.35. Essentially all (90-95%) the effluent cells were viable and 80% of these cells attached to the substratum within 1 hour. Small patches of attached cells coalesced to form confluent monolayers in 3-5 days. Confluent monolayers of endothelial cells consisted of a homogeneous population of tightly packed, polygonal cells. Selected cultures were serially subcultured (trypsin-EDTA) for 12-14 months (30-35 passages) without any apparent change in morphology or loss of growth characteristics. Primary and three-month old (15 passages) cultures had population doubling times of 32-34 hours and 29-31 hours, respectively. These cells (primary and subcultures) did not require a minimum cell number to become established in culture. Bovine endothelial cells (primary, first, fifth and thirteenth passages) were characterized ultrastructurally by the presence of Weibel-Palade bodies, pinocytotic vesicles and microfilaments and immunologically by the presence of thrombosthenin-like contractile proteins and Factor VIII antigen. The intercellular junctions of post-confluenct cultures stained specifically with silver nitrate. From these data, we concluded that identifiable endothelial cells could be obtained from bovine aortae and cultured and maintained for prolonged periods of time.

Animals↗
PubMed1978

The inhibitory effect of aspirin on human endothelial cells.

Human endothelial cell monolayers prepared from umbilical veins have been incubated with aspirin (1--2 mM) dissolved in Hepes modified solution and in platelet-rich plasma. They have also been incubated with plasma prepared from subjects before and after intake of aspirin giving a mean plasma concentration of 0.5 mM. The effects of the endothelial cells on ADP and collagen-induced platelet aggregation and malondialdehyde production in platelet-rich plasma have been tested. The endothelial cells had a spontaneous inhibitory effect on all three parameters. This effect was abolished when the cells were incubated with aspirin dissolved in MHS for 20 min and the increase in effect observed when platelet-rich plasma was incubated with endothelial cells for a period of 30 min was similarly inhibited when aspirin was dissolved in plasma or when plasma prepared from subjects who had taken aspirin were used. Aspirin had no inhibitory effect on prostacyclin (PGI2) with regard to the effect of PGI2 on platelets. On the contrary, the two compounds had an additive inhibitory effect on platelet aggregation induced by ADP and collagen. These findings should be considered with regard to the use of aspirin as an antithrombotic agent.

Aspirin↗
PubMed1977

Synthesis of prostaglandin I2 (prostacyclin) by cultured human and bovine endothelial cells.

Cultured endothelial cells derived from human umbilical veins or bovine aorta produce a potent inhibitor of platelet aggregation. The inhibitor is synthesized from sodium arachidonate or or prostaglandin endoperoxides by a microsomal enzyme system. Tranylcypromine, a specific antagonist of prostacyclin synthetase, suppresses production of the inhibitor by endothelial cells. The inhibitor, which is ether extractable, has been identified using a two-step thin-layer radiochromatographic procedure and a synthetic prostaglandin I2 standard. With this procedure, we have shown that human and bovine endothelial cells convert sodium [3H]arachidonate to radiolabeled prostaglandin I2 and 6-keto-prostaglandin F1alpha, as wellas prostaglandin E2. Thus, endothelial cells may be non-thrombogenic in vivo because they synthesize and release prostaglandin I2, a potent inhibitor of platelet aggregation.

Animals↗