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Growth of cells from esophageal squamous cell carcinoma biopsies in a reconstituted basement membrane.

Cells from esophageal carcinoma biopsies were cultured on or inside a three-dimensional basement membrane matrix (matrigel). Their growth was compared to cells derived from control esophageal biopsies. Cells from both normal and neoplastic tissue attached poorly to tissue culture plastic. Matrigel coating improved adhesion and growth. When cells were grown inside a matrigel matrix, a striking difference was noticed between carcinoma cells and controls. Carcinoma cells grew invasively in the three-dimensional substrate and digested the matrix after a few weeks; control cells did not grow and only a few necrotic cells were visible with time. Matrigel provided a better growth substrate than plastic for esophageal derived cells and discriminated between carcinoma-derived and control cells when used as a three-dimensional growth substrate. Our studies suggest a possible use of matrigel for the selective growth of tumor cells derived directly from tissue biopsies.

Basement Membrane↗

Substrate modulation of cultured rabbit conjunctival epithelial cell differentiation and morphology.

This study demonstrated that growth and differentiation of rabbit conjunctival epithelial cells could be promoted by such substrata as collagen gel, matrigel or various mixtures of collagen and matrigel in a defined culture system. On conventional plastic or glass culture, the conjunctival epithelial cells adopted a monolayer of small epithelioid cells in primary cultures. They became enlarged, squamoid and exhibited notable senescence upon subcultures. On collagen gel, cells formed an organized monolayer sheet with cuboid shape and cell polarity. On matrigel, cells formed globules with stratified appearance including the basal layer of the outer part of globule and the squamoid cells of the central part of globule. The epithelial origin of these cultures was verified by the positive immunostaining of anti-keratin monoclonal antibodies. Expression of mucin antigen was lost on plastic or glass culture, but promoted on collagen gel or matrigel, as demonstrated by staining with periodic acid Schiff's reagent and anti-mucin monoclonal antibody stainings. These results indicate that both collagen gel and matrigel can provide a permissive substrate environment for goblet cell differentiation. Furthermore, this unique phenotypic expression may be possessed only by a selective cell subpopulation. This culture system will allow us to further explore the mechanism by which the goblet cell differentiation is controlled.

Animals↗

Heterotransplantation of primary and established human tumour cells in nude mice.

Previous successful transplantations of human tumour cells into athymic nude mice have been described when cells were injected with a reconstituted basement membrane (matrigel). We have compared the development and the histology of tumours following injection with matrigel or with culture medium of a panel of tumour cells exhibiting different degrees of tumorigenicity. Two cell lines (MCF7 and MCF7/6) required matrigel in order to form tumours. When inoculated with matrigel, all the other cell lines tested [MCF7 gpt, MCF7ras, MCF7(AZ), MCF7(AZ)TD5, MDA-MB 231, HT1080] showed increased tumour take and reduced latency period. Human primary tumours (melanoma, breast and colon cancers) were transplanted successfully into nude mice, in the presence of matrigel. Breast primary tumours or cell lines gave rise to poorly differentiated carcinomas. The other tumours presented histopathological patterns typical of differentiated human cancers.

Adenocarcinoma↗

Morphogenesis of normal human salivary gland cells in vitro.

Primary cultured human salivary gland cells were transfected with ori-defective mutant DNA of SV40. Following 2-3 weeks of transfection, slowly expanding colonies consisting of small compact cells emerged, while mock-transfected cells did not grow any more and eventually entered crisis, followed by cell death. Using limited dilution technique, we isolated 4 cell clones with distinct morphology from a single colony. Morphological observation of cells cultured on plastic dishes precisely revealed the characteristics of the constituent cells of salivary gland; i.e., three cell clones showing cuboidal- (NS-SV-DC), spindle- (NS-SV-MC), and flattened morphology (NS-SV-SC) were similar to duct-, myoepithelial-, and squamous phenotype, respectively. A remaining cell clone, polygonal in shape and with numerous secretory granules (NS-SV-AC), resembled an acinar cell. Characterization of cell clones by ultrastructural examination and search for specific antigens showed the similarity of NS-SV-DC, NS-SV-MC, NS-SV-AC, and NS-SV-SC to duct, myoepithelial, acinar, and squamous cells, respectively. Anchorage-independent growth in soft agar and tumorigenicity in nude mice were not recognized in all cell clones. These results demonstrate that establishment of cell clones with duct-, myoepithelial-, acinar-, or squamous phenotype was accomplished in the in vitro system, and that based on the evaluation of colony-forming ability in soft agar and tumorigenicity in nude mice these cell clones can be considered to be non-tumorigenic. Using the above in vitro system, we examined the effect of a reconstituted basement membrane extract, Matrigel, on the morphogenesis of cultured normal human salivary gland cells. When NS-SV-DC or NS-SV-MC were seeded on Matrigel in serum-free culture conditions, they formed round or zonal clusters on day 1; failing however, to develop into a salivary gland morphogenesis. Semithin sections of cell clones cultured on Matrigel exhibited multicellular aggregates on day 1, while on days 2 and 3 these cells lost both cell-cell and cell-Matrigel interactions and eventually entered crisis. In an attempt to understand the mechanism involved in this phenomenon, we have investigated proteolytic enzymes and their inhibitors secreted by cell clones. Although cell clones produced almost identical levels of gelatinases, they released increased amounts of plasminogen activators (PAs) as compared with a neoplastic human salivary gland cell line (HSG), which had already been demonstrated to differentiate into acinar cells when cultured on Matrigel. Obvious difference of expression level of tissue inhibitor of metalloproteinases-1 (TIMP-1) was not observed in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Morphological comparison and functional reconstitution of rat hepatic parenchymal cells on various matrices.

Four types of materials, type I collagen coat (Coat), acid-soluble type I collagen gel (Hardgel), pepsin-treated acid-soluble type I collagen gel (Softgel), and an extract of extracellular matrix of the murine Engelbreth-Holm-Swarm sarcoma (Matrigel), were used as matrices to culture rat hepatic parenchymal cells, and their morphological changes and adhesion were compared to the matrices by electron microscopic observations. Hepatic parenchymal cells cultured on Coat and Hardgel were extended and flattened, whereas cells cultured on Softgel and Matrigel assembled and formed aggregates. Such aggregates consisted of several hepatic parenchymal cells, with a recognizable bile duct-like alveolus on the inside. Morphologically, the aggregates were more spherical on Matrigel and oval shaped on Softgel. Microvilli of the cell surface were parallel to the matrix on Matrigel, but invaded into the gel on Softgel. Subsequently, investigation into how these morphological features affected the liver-specific functions, including secretion of albumin and induction of P450 by 3-methylcholanthrene, demonstrated that a high level of liver function was maintained in a long-term culture in hepatic parenchymal cells on Softgel. These results suggest that hepatic parenchymal cell interactions were stronger with Softgel than with Matrigel, and that Softgel appears to closely mimic the in vivo environment.

Animals↗

Glioma invasion in vitro is mediated by CD44-hyaluronan interactions.

Invasion is a clinically important problem contributing to mortality and morbidity in patients with gliomas, but the mechanism(s) by which glioma cells invade surrounding brain structures is poorly understood. Various experimental models have been used in attempts to elucidate the process of glioma invasion. An in vitro model which is increasingly being employed involves measurement of the rate of invasion of tumour cells through Matrigel-a complex mixture of extracellular matrix components derived from the Engelbroth-Holm-Swarm (EHS) sarcoma. This model has been used to examine the possibility that extracellular hyaluronan (HA) might facilitate the invasive behaviour of human glioma cells. The major component of Matrigel is laminin, with smaller amounts of collagen IV, heparan sulphate proteoglycans, entactin, and nidogen but it lacks HA. In our experiments, we have incorporated HA into Matrigel and have measured its effect on the rate of invasion of human glioma cells in a modified Boyden chamber assay system. The incorporation of HA (50-800 mg/cm2) resulted in a dose-dependent increase in invasion. Invasion was enhanced by up to 70 per cent in comparison with HA-free Matrigel. Since CD44 is a major HA receptor expressed on gliomas, it might have a role in the HA-mediated facilitation of invasion. This was tested by blocking CD44 with specific antibody, which resulted in a 43 per cent reduction in invasion rate. We conclude that in an in vitro model system, HA enhances invasion of glioma cells and that the mechanism involves a CD44-HA interaction.

Biocompatible Materials↗

Modulation of invasive properties of murine squamous carcinoma cells by heterologous expression of cathepsin B and cystatin C.

Murine SCC-VII squamous carcinoma cells have the capacity to penetrate reconstituted basement membranes (Matrigel) in vitro. The invasion of Matrigel layers by SCC-VII cells was significantly reduced by E-64, a specific inhibitor of lysosomal cysteine proteinases. The cathepsin-B-selective E-64 derivative, CA-074, inhibited penetration of Matrigel by SCC-VII cells to the same extent, indicating a major role for this particular lysosomal enzyme in extracellular-matrix degradation during squamous-carcinoma-cell invasion. SCC-VII cells were stably transfected with a cDNA encoding human procathepsin B, in an attempt to modulate the invasive properties of the cell line. The transfected cells expressed the heterologous gene, secreted increased amounts of procathepsin B and displayed enhanced invasive potential. In vivo, the activity of cathepsin B is strictly regulated by endogenous inhibitors. SCC-VII cells were therefore also stably transfected with a cDNA encoding human cystatin C, the most potent cysteine-proteinase inhibitor in mammalian tissues. The expression of this transgene resulted in the production of active recombinant cystatin C and a pronounced reduction in Matrigel invasion. These studies demonstrate that the invasive properties of squamous-cell carcinomas can be changed by modulation of the balance between cathepsin B and its endogenous inhibitors, and provide further evidence for the involvement of this lysosomal cysteine proteinase in tumour invasion and metastasis.

Animals↗

Integrin-dependent role of human T cell matrix metalloproteinase activity in chemotaxis through a model basement membrane.

Human T lymphoblastoma cells of the CD4+ 8+ Tsup-1 line, that express alpha 4 and alpha 5 but not alpha 6 integrins of the beta 1 family, and CD4+ human blood T cells bind vasoactive intestinal peptide (VIP) with high affinity, leading to increased adherence, secretion of matrix metalloproteinases (MMPs), and chemotaxis. VIP-enhanced adherence of T cells to fibronectin was inhibited significantly by neutralizing monoclonal antibodies to beta 1 > alpha 4 > > alpha 5, but not to alpha 6. Antibodies to beta 1 and alpha 4 suppressed to a similarly significant extent VIP stimulation of both MMP-dependent T cell chemotaxis through fibronectin-enriched Matrigel and T cell degradation of 3H-type IV collagen in the Matrigel, without affecting VIP-evoked secretion of MMP by suspensions of T cells. The lesser inhibition of VIP-enhanced adherence of T cells to fibronectin by anti-alpha 5 antibody, than antibodies to beta 1 or alpha 4 chains, was associated with lesser or no suppression of MMP-dependent T cell chemotaxis through Matrigel and T cell degradation of type IV collagen in the Matrigel in response to VIP. Specific beta 1 integrins thus mediate interactions of stimulated T cells with basement membranes, including adherence, localized digestion by MMPs, and chemotactic passage, that promote entry of T cells into extravascular tissues.

Antibodies, Blocking↗

Extracellular matrix is required for skeletal muscle differentiation but not myogenin expression.

Skeletal muscle cells are a useful model for studying cell differentiation. Muscle cell differentiation is marked by myoblast proliferation followed by progressive fusion to form large multinucleated myotubes that synthesize muscle-specific proteins and contract spontaneously. The molecular analysis of myogenesis has advanced with the identification of several myogenic regulatory factors, including myod1, myd, and myogenin. These factors regulate each other's expression and that of muscle-specific proteins such as the acetylcholine receptor and acetylcholinesterase (AChE). In order to investigate the role of extracellular matrix (ECM) in myogenesis we have cultured myoblasts (C2C12) in the presence or absence of an exogenous ECM (Matrigel). In addition, we have induced differentiation of myoblasts in the presence or absence of Matrigel and/or chlorate, a specific inhibitor of proteoglycan sulfation. Our results indicated that the formation of fused myotubes and expression of AChE was stimulated by Matrigel. Treatment of myoblasts induced to differentiate with chlorate resulted in an inhibition of cell fusion and AChE activity. Chlorate treatment was also found to inhibit the deposition and assembly of ECM components such fibronectin and laminin. The expression of myogenin mRNA was observed when myoblasts were induced to differentiate, but was unaffected by the presence of Matrigel or by culture of the cells in the presence of chlorate. These results suggest that the expression of myogenin is independent of the presence of ECM, but that the presence of ECM is essential for the formation of myotubes and the expression of later muscle-specific gene products.

Acetylcholinesterase↗

Interaction between Alzheimer's disease beta A4 precursor protein (APP) and the extracellular matrix: evidence for the participation of heparan sulfate proteoglycans.

The interaction between the Alzheimer amyloid precursor protein (APP) and an intact extracellular matrix (ECM), matrigel, obtained from Engelbreth-Holm-Swarm tumors was evaluated. Based on quantitative analyses of the binding data obtained from solid phase binding assays, two binding sites on the ECM were identified for [125I]-APP (with apparent Kd1 of 1.0 x 10(-11) M and Kd2 of 1.6 x 10(-9) M respectively). Over 70% of [125I]-APP was displaced by heparin and N-desulfated heparin but not by chondroitin sulfate. Pretreatment of matrigel with heparitinase decreased the binding of [125I]-APP by 80%. beta-amyloid peptides (residues 1-40, 1-28, and 1-16) containing a heparin binding domain also displaced 80% of bound [125I]-APP, which was totally displaced by intact APP. The binding of [125I]-APP to matrigel increased by 210% with a decrease in the pH. These observations suggest that [125I]-APP interacts mainly with heparan sulfate proteoglycan present in the ECM. The binding of [125I]-APP to individual ECM components was also analyzed. [125I]-APP was found to bind laminin and collagen type IV but not fibronectin. However, when these ECM constituents were combined, the extent of APP-binding decreased significantly, to levels comparable to those obtained with intact matrigel, suggesting that multiple interactions may occur between ECM constituents and [125I]-APP. The results are discussed in terms of APP function and amyloidogenesis.

Alzheimer Disease↗

A combination of insulin-like growth factor-I and platelet-derived growth factor enhances myelination but diminishes axonal regeneration into Schwann cell grafts in the adult rat spinal cord.

Insulin-like growth factor-I (IGF-I) promotes axonal regeneration in the peripheral nervous system and this effect is enhanced by platelet-derived growth factor (PDGF). We decided, therefore, to study the effects of these factors on axonal regeneration in the adult rat spinal cord. Semipermeable polymer tubes, closed at the distal end, containing Matrigel mixed with cultured rat Schwann cells and IGF-I/PDGF, were placed at the proximal stump of the spinal cord after removal of the thoracic T9-11 segments. Control animals received implants of only Matrigel and Schwann cells or only Matrigel and IGF-I/PDGF. Four weeks after implantation, electron microscopic analysis showed that the addition of IGF-I/PDGF resulted in an increase in the myelinated:unmyelinated fiber ratio from 1:7 to 1:3 at 3 mm in the Schwann cell graft, and that myelin sheath thickness was increased 2-fold. The reduced number of unmyelinated axons was striking in electron micrographs. These results suggested that IGF-I/PDGF enhanced myelin formation of regenerated axons in Schwann cell implants, but there was a 36% decrease in the total number of myelinated axons at the 3 mm level of the graft. This finding and the altered myelinated:unmyelinated fiber ratio revealed that the overall fiber regeneration into Schwann cell implants was diminished up to 63% by IGF-I/PDGF. Histological evaluation revealed that there were more larger cavities in tissue at the proximal spinal cord-graft interface in animals receiving a Schwann cell implant with IGF-I/PDGF. Such cavitation might have contributed to the reduction in axonal ingrowth. In sum, the results indicate that whereas the combination of IGF-I and PDGF enhances myelination of regenerating spinal cord axons entering implants of Matrigel and Schwann cells after midthoracic transection, the overall regeneration of axons into such Schwann cell grafts is diminished.

Animals↗

The effect of various substrates on cell attachment and differentiation of 3T3-F442A preadipocytes.

The influence of extracellular matrix (Matrigel), collagen, and polylysine substrates on cell attachment and differentiation in 3T3-F442A preadipocytes was investigated. In comparison to an uncoated-polystyrene substrate, a concentrated Matrigel substrate (100 microg/cm2) markedly increased intracellular lipid level by about 30%, whereas a lower density Matrigel (10 microg/cm2) accelerated the differentiation rate but did not increase the amount of lipid 21 days after addition of adipogenic factors. Preadipocytes on the collagen surface differentiated less extensively than cells on the polystyrene. Polylysine did not effectively support attachment for either differentiated or undifferentiated cells. These results suggest that Matrigel provides the most suitable environment for both cell adhesion and differentiation for 3T3-F442A cells. This is in contrast to a previous report that extracellular matrix (from corneal endothelial cells) was detrimental to differentiation of 3T3-F442A cells.

3T3 Cells↗

TNF-alpha regulates mouse fetal hepatic maturation induced by oncostatin M and extracellular matrices.

Fetal hepatic maturation consists of multisteps and is regulated by several cytokines and cell-cell or cell-matrices interactions. In the mid-to-late fetal stage, hepatocytes have few metabolic functions associated with adult liver homeostasis. Cultured fetal hepatocytes acquire the expression of several mature liver-specific genes through stimulation with hepatic maturation factor oncostatin M (OSM) and matrigel. Tumor necrosis factor-alpha (TNFalpha) regulates fetal hepatic maturation stimulated by OSM and matrigel. TNFalpha suppressed expression of mature liver-specific genes such as tyrosine aminotransferase and apolipoproteins. In addition, the expression of hematopoietic cytokines and cyclin A2, repressed by OSM and matrigel, is induced by TNFalpha in the fetal hepatic cultures coincident with cell division. TNFalpha inhibited the induction of hepatocyte nuclear factor 4alpha induced by OSM and matrigel, suggesting that down-regulation of hepatocyte nuclear factor 4alpha expression is involved in the mechanism of suppression of hepatic maturation by TNFalpha. Interestingly, TNFalpha is expressed in the prenatal and postnatal liver but not in adult liver, whereas TNFR1, a TNFalpha receptor, is expressed in both fetal and adult livers. In conclusion, TNFalpha is a suppressive factor of hepatic maturation. The balance between hepatic maturation factor (OSM and extracellular matrices) and TNFalpha is important for liver development.

Animals↗

Morphological changes induced by extracellular matrix are correlated with maturation of rat small hepatocytes.

Small hepatocytes (SHs), which are known to be hepatic progenitor cells, were isolated from an adult rat liver. SHs in a colony sometimes change their shape from small to large and from flat to rising/piled-up. The aim of the present study is to clarify whether the alteration of cell shape is correlated with the maturation of SHs and whether extracellular matrix (ECM) can induce the morphological changes of SHs. We used liver-enriched transcription factors (LETFs) such as hepatocyte nuclear factor (HNF) 4 alpha, HNF6, CCAAT/enhancer binding proteins (C/EBP) alpha, and C/EBP beta, tryptophan 2,3-dioxygenase (TO), and serine dehydratase (SDH) as markers of hepatic maturation. To enrich the number of SH colonies, the colonies were isolated from dishes and replated. Replated colonies proliferated and the average number of cells per colony was about five times larger at day 9 than at day 1. When the cells were treated with laminin, type IV collagen, a mixture of laminin and type IV collagen, Matrigel or collagen gel (CG), only the cells treated with Matrigel dramatically changed their shape within several days and had reduced growth activity, whereas the cells treated with other ECM did not. HNF4 alpha, HNF6, C/EBP alpha, C/EBP beta, and TO were well expressed in the cells treated with Matrigel. Furthermore, addition of both glucagon and dexamethasone dramatically induced the expression of SDH mRNA and protein in the cells treated with Matrigel. In conclusion, morphological changes of SHs may be correlated with hepatic maturation and basement membrane (BM)-like structure may induce the morphological changes of SHs.

Animals↗

Entactin promotes adhesion and long-term maintenance of cultured regenerated skeletal myotubes.

The basal lamina protein, laminin, has been shown to promote migration and proliferation of cultured skeletal myoblasts, resulting in increased myotube formation. However, skeletal myotubes adhere poorly to a laminin substrate, and long-term cultures of skeletal myotubes on laminin have not been achieved. We have found that cultured satellite cells from bupivacaine-damaged rat skeletal muscle actively proliferate and differentiate on a diluted Matrigel substrate composed of laminin, type IV collagen, heparan sulfate proteoglycan, and entactin. Myotubes cultured on diluted Matrigel are contractile and have never been observed to detach from the culture dish; rather, myotubes generally atrophy after 2-3 weeks in culture. Antibodies directed against the various protein components of Matrigel were used to determine the role of each component in enhancing muscle differentiation. Anti-laminin impaired satellite cell adhesion, whereas antibodies against either type IV collagen or heparan sulfate proteoglycan had no effect. Anti-entactin did not inhibit attachment, proliferation, or fusion of cultured satellite cells; however, myotubes exposed to anti-entactin failed to adhere to the culture dish after spontaneous myotube contractions began. We conclude that entactin is responsible for long-term maintenance and maturation of contractile skeletal myotubes on a diluted Matrigel substrate. This is the first study to assign a biological function for entactin in myogenesis.

Animals↗

Type IV collagenase(s) and TIMPs modulate endothelial cell morphogenesis in vitro.

It has been proposed that proteases are important in endothelial cell behavior. We examined the contribution of the gelatinase/type IV collagenase system in an in vitro model of endothelial differentiation. Human umbilical vein endothelial cells rapidly align and form networks of tubes when cultured on a basement membrane preparation, Matrigel. Zymograms of culture supernates demonstrate a 72-kD and a 92-kD gelatinase activity; the cells produce most of the 72-kD gelatinase, whereas the 92-kD activity is derived entirely from the Matrigel. Addition of antibodies against type IV gelatinase/collagenase decreases the area of the tube network. Both tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2, similarly decrease tube formation when added to cultures. Conversely, exogenous recombinant 72-kD gelatinase increases tube-forming activity. The effects of the anti-gelatinase antibodies and the TIMPs are not additive. Inhibition by either antibodies or TIMPs is greatest when they are added at culture initiation, suggesting that the protease activity is important in the early steps of morphogenesis. However, culture of the cells on Matrigel does not increase early expression of mRNA for the 72-kD gelatinase. Expression of message for the enzyme actually decreases during the course of the assay, while transcription of mRNAs for TIMPs increases, further supporting the concept that collagenases facilitate an early event in tube formation. These data demonstrate that gelatinase/type IV collagenase activity is important in endothelial cell morphogenesis on Matrigel, and suggest a role for collagenases in formation of new capillaries in vivo.

Amino Acid Sequence↗

HSG cells differentiated by culture on extracellular matrix involves induction of S-adenosylmethione decarboxylase and ornithine decarboxylase.

The human salivary gland (HSG) epithelial cell line can differentiate when cultured on extracellular matrix preparations. We previously identified >30 genes upregulated by adhesion of HSG cells to extracellular matrix. In the current studies, we examined the role of one of these genes, the polyamine pathway biosynthetic enzyme S-adenosylmethionine decarboxylase (SAM-DC) and the related enzyme, ornithine decarboxylase (ODC), on HSG cell differentiation during culture on extracellular matrix. HSG cells cultured on fibronectin-, collagen I gel-, and Matrigel-coated substrates for 12-24 h upregulated SAM-DC and ODC mRNA expression and enzyme activity compared to cells cultured on non-precoated substrates. After 3-5 days, HSG cells grown on Matrigel- or collagen I gel-coated substrates acquired a differentiated phenotype: the cells showed changes in culture morphology and increased expression of salivary gland differentiation markers (vimentin, SN-cystatin, and alpha-amylase). Further, culturing the cells on substrates precoated with an anti-beta1-integrin-antibody promoted differentiation-like changes. HSG cells cultured on collagen I- or Matrigel-coated substrates rapidly entered the cell cycle but showed decreased cell proliferation at longer times. In contrast, cell proliferation was enhanced on fibronectin-coated substrates compared to cells on non-precoated substrates. Treatment with the polyamine synthesis inhibitors, difluoromethylornithine (DFMO), and methylglyoxal bis-(guanylhydrazone) (MGBG), inhibited cell proliferation and delayed (3)H-thymidine incorporation in HSG cells cultured on all of the substrates. Further, inclusion of DFMO and MGBG inhibited or delayed acquisition of the differentiated phenotype in HSG cells cultured on Matrigel- or collagen I gel-coated substrates. This suggests that the adhesion-dependent expression of SAM-DC and ODC contributes to extracellular matrix-dependent HSG cell differentiation.

Adenosylmethionine Decarboxylase↗

Effects of extracellular matrix on differentiation of mouse fetal gonads in the absence of mesonephros in vitro.

The influence of mesonephric tissues and the extracellular matrix on mouse gonadal differentiation was examined in vitro. Gonadal ridges, with or without the adjacent mesonephric region, were removed from mouse embryos on day 12 post coitum (p.c.), and cultured in the presence or absence of reconstituted basement membrane (matrigel) for 5 days. Culturing control undifferentiated testes with mesonephric tissues induced normal testicular differentiation. When testes without mesonephric tissues were cultured in the absence of matrigel, testicular cord formation was not observed in the explants. Sertoli cells were irregularly arranged in the testicular parenchyma, and no continuous basal lamina was formed around the Sertoli cells. However, when testes without mesonephric tissues were embedded in matrigel and cultured for 5 days, the Sertoli cells were organized into testicular cord-like structures. The Sertoli cells positioned at the base of the cord-like structures were closely connected to the matrigel at their basal surface, and showed a polarized distribution of vimentin filaments in their basal cytoplasm. Leydig cells, on the other hand, were differentiated in all testicular explants. In all ovarian explants, germ cells normally entered meiotic prophase. Therefore, these findings indicate that the extracellular matrix permits testicular differentiation in the absence of the mesonephros, and that removal of mesonephric tissues leads to developmental failure of cord formation because the components of the extracellular matrix around pre-Sertoli cells are incomplete.

Animals↗