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PubMed1989

Repair of microvilli in the rat small intestine after damage with lectins contained in the red kidney bean.

That microvilli of intestinal absorptive cells in the duodenum and jejunum are disrupted by acute challenge with lectins contained in raw kidney beans (RKB) was shown nearly 10 yr ago by light microscopy. However, the precise morphologic damage produced by RKB has not been characterized, and it is not known whether microvilli, once damaged, undergo repair. We have examined these issues by challenging rats with suspensions of 300 mg of RKB, boiled beans, or standard laboratory chow by orogastric lavage. Microvillus length was measured in electron micrographs from 6 to 20 h after challenge. Epithelial cell migration was determined by autoradiography after injection of [3H]thymidine. After challenge with RKB, microvilli (a) showed extensive vesiculation along the length of villi 2-4 h after challenge; (b) were reduced significantly in length along the entire villus 6 h after challenge; and (c) were near normal in length by 20 h after challenge. Microvillus length was also reduced significantly 6 h after challenge with boiled beans. The rate of cell migration was not accelerated by treatment with RKB. These data suggest that damage to microvilli caused by 300 mg of RKB is self-limited and reversible; microvilli once damaged by RKB are repaired. Repair of microvilli is due to intrinsic reparative processes rather than accelerated replacement of damaged cells. We speculate that microvilli may be repeatedly damaged and repaired after ingestion of dietary lectins.

Animals↗
PubMed2005

Microvilli defects in retinas of ezrin knockout mice.

Ezrin, a member of the ezrin/moesin/radixin (ERM) family, localizes to microvilli of epithelia in vivo, where it functions as a bridge between actin filaments and plasma membrane proteins. In the eye, ezrin has been localized to both apical microvilli of Müller cells and retinal pigment epithelium (RPE) apical microvilli and basal infoldings. In the present study, we analyze these structures in the eyes of early postnatal ezrin knockout mice. This analysis indicates that the loss of ezrin leads to substantial reductions in the apical microvilli and basal infoldings in RPE cells and in the Müller cell apical microvilli. The absence of apical microvilli in the RPE is accompanied by the presence of microvilli-like inclusions (MIs) in the RPE cytoplasm. Finally, photoreceptors in the ezrin knockout animals show substantial retardation in development as compared to their wild type littermates.

Animals↗
PubMed2004

Proteomic characterization of isolated retinal pigment epithelium microvilli.

Polarized epithelial cells are characterized by displaying compartmentalized functions associated with differential distribution of transporters, structural proteins, and signaling molecules on their apical and basolateral surfaces. Their apical surfaces frequently elaborate microvilli, which vary in structure according to the specific type and function of each epithelium. The molecular basis of this heterogeneity is poorly understood. However, differences in function will undoubtedly be reflected in the specific molecular composition of the apical surface in each epithelial subtype. We have exploited a method for isolating microvilli from the mouse eye using wheat germ agglutinin (WGA)-agarose beads to begin to understand the specific molecular composition of apical microvilli of the retinal pigment epithelium (RPE) and expand our knowledge of the potential function of this interface. Initially, apical RPE plasma membranes bound to WGA beads were processed for morphological analysis using known apical and basolateral surface markers. The protein composition of the apical microvilli was then established using proteomic analysis. Over 200 proteins were identified, including a number of proteins previously known to be localized to RPE microvilli, as well as others not known to be present at this surface. Localization of novel proteins identified with proteomics was confirmed by immunohistochemistry in both mouse and rat eye tissue. The data generated provides new information on the protein composition of the RPE apical microvilli. The isolation technique used should be amenable for isolating microvilli in other epithelia as well, allowing new insights into additional functions of this important epithelial compartment.

Animals↗
PubMed1997

Presentation of integrins on leukocyte microvilli: a role for the extracellular domain in determining membrane localization.

Adhesion of blood leukocytes to the endothelium involves multiple steps including initial attachment (tethering), rolling, and firm arrest. Presentation of adhesion molecules on leukocyte microvilli can substantially enhance tethering. Localization of L-selectin to microvilli and of CD44 to the planar cell body have been shown to depend upon their transmembrane and cytoplasmic domains. We investigated the role of leukocyte integrin transmembrane and cytoplasmic domains in initiating adhesion under flow and in microvillous localization. Integrins alpha4beta7, alphaLbeta2, and alphaMbeta2 were heterologously expressed in K562 cells. alpha4beta7 initiated adhesion under flow and localized to microvilli, whereas beta2 integrins did not initiate adhesion and localized to the cell body. Chimeric integrins were produced by replacing the alpha4beta7 cytoplasmic and/or transmembrane domains with the homologous domains of alphaLbeta2 or alphaMbeta2. Unexpectedly, these chimeras efficiently mediated adhesion to the alpha4beta7 ligand mucosal addressin cell adhesion molecule-1 under flow and localized to microvilli. Therefore, differences between the transmembrane and cytoplasmic domains of alpha4 and beta2 integrins do not account for differences in ability to support attachment under flow or in membrane localization. Integrins alpha4beta1, alpha5beta1, alpha6Abeta1, alphavbeta3, and alphaEbeta7 also localized to microvilli. Transmembrane proteins known or suspected to associate with extracellular domains of microvillous integrins, including tetraspans and CD47, were concentrated on microvilli as well. These findings suggest that interactions between the extracellular domains of integrins and associated proteins could direct the assembly of multimolecular complexes on leukocyte microvilli.

Cell Adhesion↗
PubMed1979

Regulation of surface topography of mouse peritoneal cells. Formation of microvilli and vesiculated pits on omental mesothelial cells by serum and other proteins.

The mesothelial cells of the mouse omentum provide an in vivo model for the study of the mobilization of labile microvilli on the cell surface. These mesothelial cells are sparsely covered with microvilli and large pits 150--400 nm in diameter, termed vesiculated pits. On the unstimulated cell, the microvilli average 44/100 microns2 and pits, 30/100 microns 2 of surface and they are rapidly induced to increase in number by the intraperitoneal injection of isologous mouse serum. After 2 min, microvilli increase threefold, continue to sevenfold at 30 min, and decrease to fourfold at 90 min. Vesiculated pits increased with similar kinetics. Bovine serum albumin and gamma globulin also stimulate the microvilli and pits to form, but the response is a slow, gradual rise to five- or sixfold the normal value at 90 min. Evidence indicates that multiple factors, possibly including insulin and immunoglobulins, are involved in the effect of serum. The close physical and temporal relationship between microvilli and pits suggests that a correlation exists in their mobilization by the cell and it is hypothesized that microvilli function in the regulation of the cortical microfilament network in effecting this mobilization.

Animals↗
PubMed1993

Transmission electron microscopy of microvilli of intestinal epithelial cells in celiac disease in remission and transient gluten enteropathy in children after a gluten-free diet.

The structure of microvilli of intestinal epithelial cells was investigated in 70 children: 34 with celiac disease in remission, 28 with transient gluten enteropathy after a gluten-free diet, and eight controls. Transmission electron microscopy was used to determine the mean thickness of the glycocalyx layer covering the microvilli, the mean length and width of microvilli, and the number of microvilli per 1 micron length of enterocyte surface. The structure of the glycocalyx was found to be intact, but in some children with treated celiac disease the layer of glycocalyx was either thin or absent on the surface of individual cell microvilli. In children with treated celiac disease, microvilli were statistically significantly shorter than those in children with transient gluten enteropathy and controls. Microvillous width in treated celiac disease was greater as compared with that in controls. There was no difference in the number of microvilli on the enterocyte surface in the three groups.

Biopsy↗
PubMed1998

Action of insulin on the surface morphology of hepatocytes: role of phosphatidylinositol 3-kinase in insulin-induced shape change of microvilli.

In previous studies we have shown that the insulin-responding glucose transporter isoform of 3T3-L1 adipocytes, GluT4, is almost completely located on microvilli. Furthermore, insulin caused the integration of these microvilli into the plasma membrane, suggesting that insulin-induced stimulation of glucose uptake may be due to the destruction of the cytoskeletal diffusion barrier formed by the actin filament bundle of the microvillar shaft regions [Lange et al. (1990) FEBS Lett. 261, 459-463; Lange et al. (1990) FEBS Lett. 276, 39-41]. Similar shape changes in microvilli were observed when the transport rates of adipocytes were modulated by glucose feeding or starvation. Here we demonstrate that the action of insulin on the surface morphology of hepatocytes is identical to that on 3T3L1 adipocytes; small and narrow microvilli on the surface of unstimulated hepatocytes were rapidly shortened and dilated on top of large domed surface areas. The aspect and mechanism of this effect are closely related to "membrane ruffling" induced by insulin and other growth factors. Pretreatment of hepatocytes with the PI 3-kinase inhibitor wortmannin (100 nM), which completely prevents transport stimulation by insulin in adipocytes and other cell types, also inhibited insulin-induced shape changes in microvilli on the hepatocyte surface. In contrast, vasopressin-induced microvillar shape changes in hepatocytes [Lange et al. (1997) Exp. Cell Res. 234, 486-497] were insensitive to wortmannin pretreatment. These findings indicate that PI 3-kinase products are necessary for stimulation of submembrane microfilament dynamics and that cytoskeletal reorganization is critically involved in insulin stimulation of transport processes. The mechanism of the insulin-induced cytoskeletal reorganization can be explained on the basis of the recent finding of Lu et al. [Biochemistry 35(1996) 14027-14034] that PI 3-kinase products exhibit much higher affinity for the profilin-actin complex than the primary products, PIP and PIP2. Thus, activated PI 3-kinase may direct a flux of profilin-actin complexes to the membrane locations of activated insulin receptors, where, due to the release of actin monomers after binding of profilactin to PI(3,4)P2 and PI(3,4,5)P3, massive actin polymerization is initiated. As a consequence, PI 3-kinase activation initiates a vectorial reorganization of the cellular actin system to membrane sites neighboring activated insulin receptors, giving rise to local membrane stress as visualized by extensive surface deformations and shortening of microvilli. In addition, extensive high-affinity binding of F-actin-barbed endcapping proteins enhances the cytoplasmic concentration of rapidly polymerizing filament ends. Consequently, the actin monomer concentration is lowered and the (cytoplasmic) pointed ends of the microvillar shaft bundle depolymerize and become shorter. The observations presented strengthen the previously postulated diffusion-barrier concept of glucose- and ion-uptake regulation and provide a mechanistic basis for explaining the action of insulin and other growth factors on transport processes across the plasma membrane.

Actins↗
PubMed1995

Morphological changes of microvilli on different surfaces of epithelial cells in the rat bladder treated with N-butyl-N-(4-hydroxybutyl) nitrosamine.

This study investigates morphological changes of microvilli occurring on different surfaces of epithelial cells, including luminal surfaces, intercellular surfaces, and basal cell surfaces adjacent to the basement membrane (BM), in the rat bladder treated with N-butyl-N(4-hydroxybutyl) nitrosamine (BBN) by transmission electron microscopy (TEM). The present results showed that the microvilli were observed not only on the luminal surfaces of epithelial cells but also on the intercellular surfaces and basal cell surfaces adjacent to the BM following administration of BBN. There were a variety of morphological changes of microvilli on the luminal surfaces, intercellular surfaces and basal cell surfaces adjacent to the BM, respectively. It is suggested that the microvilli occurring on the luminal surfaces may not represent characteristics of the microvilli occurring on the intercellular surfaces and on the basal cell surfaces adjacent to the BM, and that occurrence of the microvilli on the epithelial cell surfaces may reflect a higher metabolic activity of proliferative epithelial cells and may play an important role in the processes of tumor growth during bladder carcinogenesis.

Animals↗
PubMed2005

Senescence marker protein-30 (SMP30) induces formation of microvilli and bile canaliculi in Hep G2 cells.

Senescence marker protein-30 (SMP30) is an androgen-independent factor that decreases with aging. To elucidate the physiological functions of SMP30, we transfected human SMP30 cDNA into the human hepatoma cell line, Hep G2. These Hep G2/SMP30 transfectants, which stably expressed large amounts of SMP30, proliferated at a slower rate and synthesized less DNA than mock transfectants (Hep G2/pcDNA3 controls). Thus, enhanced expression of SMP30 retarded the growth of Hep G2/SMP30 cells. Ultrastructural studies by scanning electron microscopy revealed numerous microvilli covering the surfaces of Hep G2/SMP30 cells, whereas few microvilli appeared on control cells. Subsequently, transmission electron microscopy revealed that groups of Hep G2/SMP30 cells exhibited bile canaliculi and possessed specialized adhesion contacts, such as tight junctions and desmosomes, at interplasmic membranes. However, in controls, units of only two cells were seen, and these lacked specialized adhesion junctions. Moesin and ZO-1 are known to be concentrated in microvilli and at tight junctions, respectively. Double-immunostaining was performed to examine whether moesin and ZO-1 were expressed in bile canaliculi with microvilli at the apical regions of Hep G2/SMP30 cells. The intensity of moesin and ZO-1 staining in the contact regions of each cell was markedly higher in Hep G2/SMP30 than in control cells. Moreover, moesin stained more interior areas, which corresponded to the microvilli of bile canaliculi. Clearly, bile canaliculi with microvilli formed at the apical ends of Hep G2/SMP30 cells. These results indicate that SMP30 has an important physiological function as a participant in cell-to-cell interactions and imply that the down-regulation of SMP30 during the aging process contributes to the deterioration of cellular interactivity.

Bile Canaliculi↗
PubMed2001

Dynamic contact forces on leukocyte microvilli and their penetration of the endothelial glycocalyx.

We develop a theoretical model to examine the combined effect of gravity and microvillus length heterogeneity on tip contact force (F(m)(z)) during free rolling in vitro, including the initiation of L-, P-, and E-selectin tethers and the threshold behavior at low shear. F (m)(z) grows nonlinearly with shear. At shear stress of 1 dyn/cm(2), F(m)(z) is one to two orders of magnitude greater than the 0.1 pN force for gravitational settling without flow. At shear stresses > 0.2 dyn/cm(2) only the longest microvilli contact the substrate; hence at the shear threshold (0.4 dyn/cm(2) for L-selectin), only 5% of microvilli can initiate tethering interaction. The characteristic time for tip contact is surprisingly short, typically 0.1-1 ms. This model is then applied in vivo to explore the free-rolling interaction of leukocyte microvilli with endothelial glycocalyx and the necessary conditions for glycocalyx penetration to initiate cell rolling. The model predicts that for arteriolar capillaries even the longest microvilli cannot initiate rolling, except in regions of low shear or flow reversal. In postcapillary venules, where shear stress is approximately 2 dyn/cm(2), tethering interactions are highly likely, provided that there are some relatively long microvilli. Once tethering is initiated, rolling tends to ensue because F(m)(z) and contact duration will both increase substantially to facilitate glycocalyx penetration by the shorter microvilli.

Animals↗
PubMed1998

Increase in expression and activity of thrombomodulin in term human syncytiotrophoblast microvilli.

A comparative study of thrombomodulin (TM), a potent natural anticoagulant, was performed in first trimester and term human placentae. Immunoreactive TM was observed on fetal vascular endothelium and syncytiotrophoblast at both gestational ages. Staining was stronger in term than in early placentae, particularly along the microvillous apical membrane of the syncytiotrophoblast. Similarly, a higher level of TM mRNA was detected by RT-PCR (P<0.02) and Northern blot analysis in extracts of whole term placentae. The localization of TM on syncytial microvilli was confirmed by electron microscopy after immunogold labelling. When isolated microvilli were compared at both gestational ages; a significant 2.3-fold increase in TM protein was observed in term microvilli as compared to first trimester microvilli by Western blot analysis (P<0.005) and ELISA (P<0.05). This higher level of TM in term microvilli was associated with an increase in its ability to activate protein C, from 3.7 +/- 1.2 to 8.7 +/- 4.2 mOD/min/microg protein +/- s.d. (P<0.01) in first trimester and term microvilli, respectively. The modulation of biologically active TM at the syncytial membrane exposed to maternal blood according to the length of gestation suggests that TM may be involved both in maternal haemostasis within the intervillous spaces, and also in the trophoblast differentiation process.

Base Sequence↗
PubMed1999

Ezrin promotes morphogenesis of apical microvilli and basal infoldings in retinal pigment epithelium.

Ezrin, a member of the ezrin/radixin/moesin (ERM) family, localizes to microvilli of epithelia in vivo, where it bridges actin filaments and plasma membrane proteins. Here, we demonstrate two specific morphogenetic roles of ezrin in the retinal pigment epithelium (RPE), i.e., the formation of very long apical microvilli and of elaborate basal infoldings typical of these cells, and characterize the role of ezrin in these processes using antisense and transfection approaches. In the adult rat RPE, only ezrin (no moesin or radixin) was detected at high levels by immunofluorescence and immunoelectron microscopy at microvilli and basal infoldings. At the time when these morphological differentiations develop, in the first two weeks after birth, ezrin levels increased fourfold to adult levels. Addition of ezrin antisense oligonucleotides to primary cultures of rat RPE drastically decreased both apical microvilli and basal infoldings. Transfection of ezrin cDNA into the RPE-J cell line, which has only trace amounts of ezrin and moesin, sparse and stubby apical microvilli, and no basal infoldings, induced maturation of microvilli and the formation of basal infoldings without changing moesin expression levels. Taken together, the results indicate that ezrin is a major determinant in the maturation of surface differentiations of RPE independently of other ERM family members.

Animals↗
PubMed2004

Microvilli structures on B lymphocytes: inducible functional domains?

Interactive contact between B lymphocytes and T cells is necessary for their expansion during an immune response. It has been shown that B lymphocytes receive signals from T cells, such as IL-4 and cross-linking of CD40, which are crucial for their differentiation. We previously found that these factors induce formation of microvilli on B cells and that this was correlated with increased homotypic adhesion of B lymphocytes. In this study we have investigated if IL-4 induce segregation of proteins to microvilli and lipid rafts. Using immuno-electron microscopy we analyzed cell-surface distribution of molecules involved in B-T cell co-activation. Recruitment to detergent-resistant membrane fractions was analyzed using sucrose gradient centrifugation. We found that microvilli were enriched in ICAM-1 and MHC class II molecules. In contrast, LFA-1 and CD40 were more abundant on the smooth cell surfaces, while B7-2 (CD86) was randomly distributed. We also discovered that depletion of cholesterol, using beta-methyl-cyclodextrin, lowered the number of microvilli, indicating that intact lipid rafts are required for their expression. Moreover, activation of B lymphocytes by lipopolysaccharide (LPS) induced increased expression of GM(1), a marker for lipid rafts. However, although both surface and total levels of GM(1) were similar in B lymphocytes stimulated with either LPS or LPS plus IL-4, GM(1) was mainly expressed on microvilli in LPS plus IL-4-stimulated cells. Taken together, our results indicate that microvilli represent distinct inducible membrane domains that can regulate direct cell-cell interactions via grouping and three-dimensional presentation of cell-surface receptors.

Animals↗
PubMed1990

Correlation between the presence of microvilli and the growth or metastatic potential of tumor cells.

We used an electron microscope to examine microvilli which appear on the surfaces of various tumor cells with high or low growth potential and/or metastatic ability. The results show that a greater number of microvilli appeared on the surfaces of tumor cells (QRpP and ERpP) which possess high growth potential than on tumor cells (QR and ER) with low growth potential. We also observed that microvilli were more abundant on the surface of highly metastatic clone cells, i.e. c-SST-2 (cl-2), mouse B16 melanoma (F-10) and human colon carcinoma (KM12SM) than on weakly metastatic clone cells, c-SST-2 (cl-4-2), B16 (F-1) and (KM12C). At the same time, more microvilli were observed on the surface of B16 BL6 cells, which were obtained from the metastatic site of the B16 F10 cells, than on the surface of the parent B16 F10 cells. Immunoelectron microscopy revealed that the c-neu oncogene product, which is closely related to an epidermal growth factor receptor, was positively stained in the microvilli of tumor cells (ERpP) with high growth potential and high metastatic ability, whereas the tumor cells (ER) with low growth potential and weak metastatic ability were not stained. These findings suggest that the increased presence of microvilli correlates closely with the growth potential and metastatic ability of tumor cells.

Animals↗
PubMed2000

A hydrodynamic mechanosensory hypothesis for brush border microvilli.

In the proximal tubule of the kidney, Na(+) and HCO(3)(-) reabsorption vary proportionally with changes in axial flow rate. This feature is a critical component of glomerulotubular balance, but the basic mechanism by which the tubule epithelial cells sense axial flow remains unexplained. We propose that the microvilli, which constitute the brush border, are physically suitable to act as a mechanosensor of fluid flow. To examine this hypothesis quantitatively, we have developed an elastohydrodynamic model to predict the forces and torques along each microvillus and its resulting elastic bending deformation. This model indicates that: 1) the spacing of the microvilli is so dense that there is virtually no axial velocity within the brush border and that drag forces on the microvilli are at least 200 times greater than the shear force on the cell's apical membrane at the base of the microvilli; 2) of the total drag on a 2.5-microm microvillus, 74% appears within 0.2 microm from the tip; and 3) assuming that the structural strength of the microvillus derives from its axial actin filaments, then a luminal fluid flow of 30 nl/min produces a deflection of the microvillus tip which varies from about 1 to 5% of its 90-nm diameter, depending on the microvilli length. The microvilli thus appear as a set of stiff bristles, in a configuration in which changes in drag will produce maximal torque.

Animals↗
PubMed2004

Lymphocyte microvilli are dynamic, actin-dependent structures that do not require Wiskott-Aldrich syndrome protein (WASp) for their morphology.

Short microvilli cover the surfaces of circulating mammalian lymphocytes. The surfaces of monocytes and neutrophils are very different, containing ruffles as their predominant structure. In this study, we present the first quantitative characterization of lymphocyte microvilli. From analysis of scanning electron micrographs, we find that median microvillar length and surface density range from 0.3 to 0.4 microm and 2 to 4 microvilli/microm(2), respectively, on lymphocytes from a variety of sources. As with similar structures from other cells, lymphocyte microvilli contain parallel bundles of actin filaments. Lymphocyte microvilli rapidly disassemble when exposed to the actin-sequestering molecule, Latrunculin A. This disassembly parallels cellular actin filament depolymerization and is complete within 2 minutes, suggesting that lymphocyte microvilli undergo continuous assembly and disassembly. In contrast to previous reports suggesting lymphocyte microvillar density to be reduced on lymphocytes from Wiskott-Aldrich syndrome (WAS) patient, we find no such deficiency in either mouse or human WAS protein (WASp)-deficient lymphocytes. These results suggest that WASp is either not involved in or is redundant in the rapid dynamics of lymphocyte microvilli.

Actins↗
PubMed1983

Functional design of microvilli in the Malpighian tubules of the insect Rhodnius prolixus.

The Malpighian tubules of Rhodnius prolixus are divided into two regions; the upper tubule, which is the site of isosmotic secretion and haemolymph filtration, and the lower tubule where water and KCl are resorbed. In the upper tubule the microvilli are arranged in clumps consisting of several hundred microvilli lying closely parallel. The microvillar plasma membranes do not touch but are held approximately equal to 16 nm apart along the full length of the microvilli. As a consequence, the extracellular space between the microvilli consists of long narrow channels. A morphometric analysis of extracellular, cytoplasmic, endoplasmic reticular and mitochondrial volume within the clumps was conducted. Using the secretion rate of the epithelium and the channel dimensions, it was calculated that the mean residence time for secreted fluid in the intermicrovillar spaces was approximately equal to 0.4s. In view of our current knowledge of the physiology and morphology of the upper tubule, it is argued: (1) that osmotically driven water passes principally through the cells, not the junctional spaces; and (2) that the microvillar clumps are a morphological specialization, which serves to maximize solute-water coupling in the upper tubule. The microvilli in the lower tubule are free-standing, with no pattern of clumping as in the upper tubule. The axopods are about twice as long as the microvilli (10-14 micron) and are found in all regions of the lower tubule. This is in agreement with the proposal that the motile axopods serve to propel uric acid crystals through the lower tubule. No morphological difference was found between the upper and lower halves of the lower tubule, although the two portions are known to be physiologically distinct.

Animals↗
PubMed1983

Pemphigus serum-induced loss of microvilli from human epidermal cells.

Scanning electron microscopic examination of human epidermal cells prepared from suction blister roofs by treatment with trypsin and dithioerythritol and incubated (37 degrees C, 18 hours) with pemphigus sera revealed a smooth or wrinkled surface texture in 83 to 96% and surface microvilli in only 17 to 4%. The disappearance of microvilli was not affected by the presence of complement. In the control specimen 54% of the cells retained their microvilli. The difference between cells incubated with pemphigus and those incubated with control sera was highly significant (p less than 0.001). Epidermal cell suspensions were also incubated with pemphigus vulgaris sera plus a protease inhibitor (ovomucoid). The loss of microvilli from human epidermal cells induced by pemphigus vulgaris serum was highly significantly inhibited by ovomucoid (p less than 0.001). The results suggest that the loss of microvilli induced by pemphigus sera, irrespective of the presence of complement, may be an important factor in acantholysis of pemphigus. Proteolytic enzymes may be responsible for the loss of microvilli and smoothing of the cell surface of human epidermal cells in vitro.

Acantholysis↗