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At least 19 recordsLinked to original sources
PubMed2003

A high endothelial venule secretory protein, mac25/angiomodulin, interacts with multiple high endothelial venule-associated molecules including chemokines.

We previously reported that mac25/angiomodulin (AGM), a 30-kDa secretory protein, is abundantly expressed in high endothelial venules (HEVs), which play a crucial role in lymphocyte trafficking to the lymph nodes and Peyer's patches. We report that mac25/AGM interacts preferentially with certain molecules that are expressed in or around HEVs. In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5). The binding of mac25/AGM to SLC and IP-10 was dose-dependent and saturable. The binding to IP-10 could be inhibited by SLC but not by a non-mac25/AGM-binding chemokine, EBI1-ligand chemokine (ELC; CCL19). Interestingly, mac25/AGM failed to interact with 18 other chemokines, suggesting that it binds to certain chemokines preferentially. Immunohistochemical analysis indicated that mac25/AGM colocalizes at least partially with SLC and IP-10 at the basal lamina of HEVs. Upon binding with mac25/AGM, SLC and IP-10 retained all their Ca(2+)-signaling activity in vitro, suggesting that mac25/AGM can hold and present chemokines in the basal lamina of HEVs. These results imply that mac25/AGM plays a multifunctional role, serving not only as an adhesion protein to interact with glycosaminoglycans and extracellular matrix proteins but also as a molecule to present chemokines so that lymphocytes extravasating through HEVs receive further directional cues subsequent to the luminal encounter with lymphoid chemokines.

Amino Acid Sequence↗
PubMed2003

Cutting edge: the B cell chemokine CXC chemokine ligand 13/B lymphocyte chemoattractant is expressed in the high endothelial venules of lymph nodes and Peyer's patches and affects B cell trafficking across high endothelial venules.

While CCR7 ligands direct T cell trafficking into lymph nodes (LNs) and Peyer's patches (PPs), chemokines that regulate B cell trafficking across high endothelial venules (HEVs) remain to be fully elucidated. Here we report that CXC chemokine ligand (CXCL)13 (B lymphocyte chemoattractant) is detected immunohistologically in the majority of HEVs in LNs and PPs of nonimmunized mice. Systemically administered anti-CXCL13 Ab bound to the surface of approximately 50% of HEVs in LNs and PPs, but not to other types of blood vessels, indicating that CXCL13 is expressed in the HEV lumen. In CXCL13-null mice, B cells rarely adhered to PP HEVs, whereas T cells did efficiently. Superfusion of CXCL13-null PPs with CXCL13 restored the luminal presentation of CXCL13 and also B cell arrest in PP HEVs at least partially. Collectively, these results indicate that CXCL13 expressed in the HEV lumen plays a crucial role in B cell trafficking into secondary lymphoid tissues such as PPs.

Animals↗
PubMed2004

Detection of a sulfotransferase (HEC-GlcNAc6ST) in high endothelial venules of lymph nodes and in high endothelial venule-like vessels within ectopic lymphoid aggregates: relationship to the MECA-79 epitope.

The interaction of L-selectin on lymphocytes with sulfated ligands on high endothelial venules (HEVs) of lymph nodes results in lymphocyte rolling and is essential for lymphocyte homing. The MECA-79 monoclonal antibody reports HEV-expressed ligands for L-selectin by recognizing a critical sulfation-dependent determinant on these ligands. HEC-GlcNAc6ST, a HEV-localized sulfotransferase, is essential for the elaboration of functional ligands within lymph nodes, as well as the generation of the MECA-79 epitope. Here, we use an antibody against murine HEC-GlcNAc6ST to study its expression in relationship to the MECA-79 epitope. In lymph nodes, the enzyme is expressed in the Golgi apparatus of high endothelial cells, in close correspondence with luminal staining by MECA-79. In lymph node HEVs of HEC-GlcNAc6ST-null mice, luminal staining by MECA-79 is almost abolished, whereas abluminal staining persists although reduced in intensity. HEV-like vessels in several examples of inflammation-associated lymphoid neogenesis, including nonobese diabetic mice, also exhibit concomitant expression of the sulfotransferase and luminal MECA-79 reactivity. The correlation extends to ectopic lymphoid aggregates within the pancreas of RIP-BLC mice, in which CXCL13 is expressed in islets. Analysis of the progeny of RIP-BLC by HEC-GlcNAc6ST-null mice establishes that the enzyme is responsible for the MECA-79 defined luminal ligands.

Animals↗
PubMed1994

High endothelial venules and cell adhesion molecules in B-cell chronic lymphocytic leukaemia and related low grade B-cell lymphoma/leukaemia: I. High endothelial venules and lymphocyte migration.

The high endothelial venule (HEV)-content and the lymphocyte migration index (LMI) of reactive lymph nodes and lymph nodes from patients with B-cell chronic lymphocytic leukaemia (B-CLL), as well as some related B-cell malignancies (lymphocytic lymphoma -LL-, prolymphocytic leukaemia -PLL-) were determined and statistically analyzed. The HEV-content and the LMI were significantly higher in reactive lymph nodes than in the low grade B-cell lymphomas and leukaemias (p < 0.001). The number of HEVs among lymphoma/leukaemia cases was the highest in LL independently of the maturation. However, the maturation of the process seems to determine the intensity of lymphocyte migration; i.e. a significantly higher LMI was found in mature (B-CLL, PF, mature; M and LL, M) than in immature subtypes (B-CLL, PF, immature -IM-; diffuse -D- and LL, IM) subtypes (levels of significance varied from p < 0.05 to p < 0.001). Based on these findings, a more intense migration of lymphocytes from blood to peripheral lymph nodes may be supposed in LL than in B-CLL, thus explaining the nodal sites of involvement in LL and the peripheral blood in B-CLL. Within the same histological categories the morphometric features in mature subtypes may implicate an enhanced HEV-lymphocyte interaction when compared to the immature subtypes.

Cell Adhesion Molecules↗
PubMed1996

Nitric oxide reduces tumor cell adhesion to isolated rat postcapillary venules.

Adhesion of circulating tumor cells to microvascular endothelium plays an important role in tumor metastasis to distant organs. The purpose of this study was to determine whether nitric oxide (NO) would attenuate tumor cell adhesion (TCA) to naive or lipopolysaccharide (LPS)-treated postcapillary venules. A melanoma cell line, RPMI 1846, was shown to be much more adhesive to postcapillary venules isolated from rat mesentery than to corresponding precapillary arterioles. Although venules exposed to LPS for 4 h demonstrated an increased adhesivity for the melanoma cells, TCA to LPS-treated arterioles was not altered. Isolated venules exposed to DETA/NO (1 mM), an NO donor, for 30 min prior to tumor cell perfusion prevented the increment in adhesion induced by LPS and attenuated TCA to naive postcapillary venules. While L-arginine (100 microM), an NO precursor, failed to decrease TCA to naive postcapillary venules, this treatment abolished LPS-stimulated TCA to postcapillary venules. The effect of L-arginine was reversed by administration of N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 microM), an NO synthase (NOS) inhibitor. These observations indicate that both exogenous and endogenous NO modulate TCA to postcapillary venules. To assess the role of NO-induced activation of cGMP in the reduction in TCA produced by DETA/NO, two additional series of experiments were conducted. In the first series, LY-83583 (10 microM), a guanylyl cyclase inhibitor, was shown to completely reverse the effect of DETA/NO on TCA to both naive and LPS-activated postcapillary venules. On the other hand, administration of 8-bromoguanosine 3',5'-cyclic monophosphate (8-B-cGMP) (1 mM), a cell permeant cGMP analog, mimicked the effect of DETA/NO and reduced TCA to LPS-stimulated postcapillary venules. These data suggest that (a) tumor cells are more likely to adhere to postcapillary venules than to corresponding precapillary arterioles, (b) LPS enhances TCA to postcapillary venules, (c) both exogenously applied (DETA/NO) and endogenously generated (L-arginine) NO attenuate the enhanced adhesion induced by LPS, but only DETA/NO reduced TCA to naive postcapillary venules, and (d) the NO-induced reduction in TCA to LPS-activated postcapillary venules occurs by a cGMP-dependent mechanism.

Aminoquinolines↗
PubMed1993

Responses of porcine epicardial venules to neurohumoral substances.

OBJECTIVE: The coronary microvenous system may be determinant of ventricular distensibility and of resistance to coronary flow under conditions of arteriolar dilatation. Because responses of venules have not been well defined, in vitro responses of porcine venules and arterioles to neurohumoral substances were examined. METHODS: Porcine subepicardial venules (125-250 microns in diameter) and arterioles (100-200 microns in diameter) were studied in a pressurised no flow state with video microscopical imaging and electronic dimension analysis. After precontraction of vessels with the thromboxane A2 analogue U46619, agents were applied extraluminally. RESULTS: Responses of precontracted venules to sodium nitroprusside, adenosine, and adenosine 5' diphosphate (ADP) were comparable with those of similarly sized arterioles. By contrast, precontracted venules responded minimally to noradrenaline, whereas arterioles were dilated potently by this agent. Precontracted arterioles were dilated minimally by serotonin and were contracted slightly by acetylcholine, whereas venules dilated in response to either serotonin or acetylcholine. Serotonin and acetylcholine both produced greater contraction in non-precontracted arterioles than in non-precontracted venules. Responses of venules to most substances were minimally affected by changes in oxygen tension except when this was very low. Relaxation of venules by ADP, serotonin, and acetylcholine were all inhibited to varying degrees by indomethacin, methylene blue, and NG-methyl-L-arginine (L-NMMA). Both methylene blue and L-NMMA produced minimal but significant contraction of non-precontracted venules, indicating a small amount of basal release of endothelium derived relaxing factor. CONCLUSION: Responses of coronary venules to acetylcholine, serotonin, and noradrenaline are opposite or of a significantly different magnitude when compared with the respective arteriolar responses. Relaxation of venules to ADP, serotonin, and acetylcholine is likely mediated at least in part by the release of endothelium derived relaxing factor and prostaglandins.

Acetylcholine↗
PubMed1988

Neurogenic inflammation in the rat trachea. I. Changes in venules, leucocytes and epithelial cells.

This study was done to characterize the morphological changes in the respiratory mucosa that occur in neurogenic inflammation, which is a type of inflammation mediated by substances released from sensory nerves. Neurogenic inflammation was produced in the trachea and bronchi of atropine-treated Long-Evans rats by electrically stimulating the left or right superior laryngeal and vagus nerves. This procedure is known to increase vascular permeability in the airways, presumably as a consequence of antidromic activation of sensory vagal axons (Lundberg & Saria, 1982). By using a particulate tracer (Monastral blue, 30 mg kg-1 i.v.) that does not cross the walls of normal tracheal blood vessels but does cross the endothelium of abnormally permeable vessels, it was possible to identify which blood vessels were affected in neurogenic inflammation. Light and electron microscopic examination of tracheas prepared after 2 or 5 min of vagal stimulation revealed that postcapillary venules and collecting venules 7-80 micron in diameter were labelled by extravasated Monastral blue but capillaries, arterioles, and larger venules were not. Venules from which the extravasation occurred had gaps as wide as 1.5 micron between endothelial cells. Most of the abnormally permeable venules were located just beneath the airway epithelium in regions between the cartilaginous rings. Extravasation also occurred from venules in the mucosa overlying the posterior membrane of the extrathoracic trachea, but little occurred in the posterior membrane of the intrathoracic trachea. After unilateral vagal stimulation, vascular permeability was increased on both sides of the trachea; it was also increased in first through fourth order bronchi but only on the side of stimulation. Leucocytes (principally monocytes and neutrophils) were adherent to the endothelium of some of the abnormally permeable venules. Erythrocytes and platelets also were adherent to the walls of some venules. These changes in venules were accompanied by a degranulation of epithelial secretory cells, widening of the spaces between tracheal epithelial cells, and probably an increase in epithelial permeability. Neurogenic inflammation in the trachea and bronchi of rats is thus characterized by increased permeability of postcapillary venules and collecting venules in specific regions of the respiratory mucosa as well as adherence of leucocytes, erythrocytes and platelets to the endothelium of these venules and prominent changes in the respiratory epithelium.

Animals↗
PubMed1972

The initiation of platelet thrombi in normal venules and its acceleration by histamine.

1. In cheek pouch preparations of anaesthetized hamsters, platelet thrombi or ;white bodies' were produced in venules by the micro-ionto-phoretic application of adenosine diphosphate (ADP). Currents of 10-400nA were passed through micropipettes containing 10 mM-ADP, the tips of which were less than 5 mu from the outer wall of the venule. The effect was quantitated by determining the time between starting the currents and the first appearance of platelets adhering inside the venule opposite the tip of the micropipette.2. Repeated applications of ADP to the same site on a venule caused the appearance of white bodies after intervals which were almost constant for up to 3 hr.3. The time to first appearance of a white body was inversely related to the iontophoretic current between about 10 and 200 nA. Currents smaller than 10 nA had no effect on the platelets. With currents of 200 nA or more the time remained at a minimum of less than 20 sec.4. With currents of about 300 nA the minimum time increased little as the pipette tip was withdrawn up to 20 mu from the venule; with greater distances the time increased progressively.5. Histamine caused gaps to appear between endothelial cells in cheek pouch venules. Histamine at a concentration of 10 mM in micropipettes was applied iontophoretically by currents of 300 nA to venules at the same sites as ADP. Histamine alone had no effect on circulating platelets. When applied before and together with ADP, histamine decreased the time to first appearance of white bodies by up to 40% below that determined with ADP alone. Iontophoretically applied histamine did not alter the mean blood flow velocity in the venules.6. After stopping the application of histamine, the time to first appearance of white bodies produced by ADP increased again in about 5 min to the control values.7. Bradykinin, which does not cause endothelial gaps in cheek pouch venules, did not accelerate the induction of white bodies like histamine.8. There were no microscopic abnormalities in venules in which white bodies had formed. Venules exposed to histamine accumulated circulating carbon particles in discrete wall areas.9. It is concluded that adhering white bodies can be induced repeatedly in normal venules by direct action of externally applied ADP on circulating platelets and that the accelerating effect of histamine on white body formation is due to the separation of endothelial cells which accelerates the inward diffusion of ADP.

Adenine Nucleotides↗
PubMed1996

Permeability-related changes revealed at endothelial cell borders in inflamed venules by lectin binding.

Plasma leakage in inflammation results from intercellular gaps that form in the endothelium of venules. These gaps and related morphological changes in endothelial cells are not readily seen by light microscopy. In this study we sought to visualize such changes by using the selective binding properties of plant lectins. Acute inflammation was induced in the trachea of pathogen-free F344 rats by injecting substance P intravenously, and 1, 3, or 10 min later the vasculature was perfused with fixative followed by a biotinylated lectin. Lectin binding was localized by avidinbiotin complex-peroxidase histochemistry and viewed in tracheal whole mounts by differential-interference contrast microscopy. The binding patterns of the 20 lectins tested fell into 4 groups. Most of the lectins either bound uniformly to the endothelium of normal and inflamed venules (group 1, e.g., Lycopersicon esculentum lectin) or bound weakly or not at all to venules (group 2, e.g., Maackia amurensis I lectin). The uniform binding of group 1 lectins not only revealed the overall vascular architecture but also made visible intercellular gaps and fingerlike processes at endothelial cell borders in inflamed venules. In postcapillary venules after substance P, the fingerlike processes were present along an average of 32% of the endothelial cell perimeter at 1 min, 25% at 3 min, and 7% at 10 min, compared with a baseline value of 2%. A third group of lectins (group 3, e.g., concanavalin A) bound selectively to focal patches of inflamed venules but bound weakly to normal venules. The fourth group (group 4, e.g., Ricinus communis I lectin) bound preferentially to focal patches in inflamed venules and also bound uniformly to normal venules. The focal binding of group 3 and 4 lectins coincided with sites of plasma leakage marked by extravasation of the particulate tracer monastral blue and was associated with subendothelial components of the vessel wall. We conclude that selected lectins reveal novel features of focal sites of plasma leakage, endothelial gaps, and fingerlike processes at endothelial cell borders in inflamed venules.

Animals↗
PubMed1978

Ultrastructure of venules in the cat brain.

Intracerebral venules of the cat were examined to establish criteria for a distinct separation between the venous and arterial system, and to characterize, in greater detail, the mural construction of individual venules. The intracerebral venules compared with those of other organs. Venules do not have a vascular wall composed clearly of endothelium, media, and adventitia, as is characteristic of arteries and arterioles. The venous endothlium has a similar structure to that of capillaries. The periendothelial cells of the venule differ in shape depending on the vascular diameter. The number of periendothelial cell processes in postcapillary venules increases progressively. Segments in which the basal lamina of the endothelium merges with that of the glia cover a smaller portion of the circumference than in venous capillary loops. In collecting venules, the endothelium is almost completely enveloped by periendothelial cells which have a larger number of filaments. There are no typical smooth muscle cells in the intracerebral venules. The perivascular space becomes wider in collecting venules, contains adventitial cells, phagocytes and a great number of collagen fibers.

Animals↗
PubMed2002

Collecting and paramuscular venules in glandular mucosa of rat stomach.

Blood from the rat gastric mucosa is drained by collecting venules running from the subepithelial layer towards the lamina muscularis mucosae. Details of their structure were studied in translucent, flat strips of the glandular stomach, in thick sections of glandular mucosa cleared in mineral oil and in semi-thin plastic sections. The number and dimensions of collecting venule outlets revealed in flat strips of gastric mucosa increased after administration of atropine and papaverine and intravital ligation of the portal vein in comparison with that of intact animals or animals with intravitally ligated portal vein but without administration of relaxing agents. In hyperemic mucosa short venules running parallel to the lamina muscularis mucosae (paramuscular venules) and draining collecting venules were distinctly visible. Saccular outlets equipped with triangular protrusions usually intervened between these vessels, probably directing blood flow. Collecting venules were straight, curved, extended or two-armed. Furthermore, numerous collecting venules contained circumscribed dilatations (sacculi) connected with the lumen of the collecting venule. Connection of paramuscular and submucosal veins occurred within the muscularis mucosae. Thus, contraction of the muscularis mucosae might control the outflow of venous blood from the gastric mucosa. Conceivably, alternate contraction and relaxation of muscularis mucosae could cause expansion and collapse of collecting venules which, in turn, would facilitate the movement of glandular content to the surface of the stomach and/or movement of interstitial fluid between cells.

Animals↗
PubMed1997

Central venulitis in the allograft liver: a clinicopathologic study.

BACKGROUND: Central venulitis denotes a histologic lesion of the allograft liver characterized by perivenular and subendothelial mononuclear inflammation of the terminal hepatic venules associated with varying degrees of perivenular hepatocyte dropout. Although this lesion has generally been considered a manifestation of acute rejection, some have suggested that it instead represents tacrolimus hepatotoxicity. METHODS: We therefore compared the clinicopathologic features of 30 episodes of isolated central venulitis with 22 episodes of combined central venulitis and typical portal acute rejection occurring in 27 patients. Nineteen of the patients received tacrolimus and eight received cyclosporine as primary immunosuppression. RESULTS: No significant differences were found between the two groups, except that isolated central venulitis more often displayed a mild inflammatory component (P=0.007) with small lymphocytes as the predominant cell type (P=0.002). None of the patients had tacrolimus or cyclosporine levels that exceeded the therapeutic range, and none had other clinical evidence of drug toxicity. Usual antirejection therapy was instituted in all but two episodes; response was evident in 93% (28 of 30) of the isolated central venulitis and 86% (19 of 22) of the central venulitis-portal acute rejection group, with histologic regression documented in all follow-up specimens (four and five, respectively). Due to persistent central venulitis, two cyclosporine patients were switched to tacrolimus, with prompt resolution. CONCLUSIONS: These findings are inconsistent with the concept that central venulitis represents drug toxicity and indicate instead that it is a form of acute allograft rejection.

Adult↗
PubMed1984

Direct observations of muscle arterioles and venules following contraction of skeletal muscle fibres in the rat.

Direct observations have been made of responses of individual arterioles and venules of rat spinotrapezius muscle to contraction of the skeletal muscle fibres. Stimuli of 4-6 V intensity, 0.1 ms duration, delivered via a micro-electrode inserted into the spinotrapezius, evoked contraction of a small bundle of skeletal muscle fibres, followed by vasodilatation which was limited to all those arterioles and venules which crossed or ran alongside activated muscle fibres. Since venules outside the region of contraction, but supplied by dilating arterioles, were not passively distended by the attendant rise in intravascular pressure, it is concluded that both the arterioles and venules dilated actively in response to muscle contraction. All arterioles responded to a single twitch contraction, the terminal arterioles (7-13 micron i.d.) showing the largest increase in diameter. Collecting venules (9-18 micron i.d.) responded to just two twitches in 1 s and larger venules to five twitches in 1 s. When twitch contractions were continuously evoked for 10 s, the responses in individual arterioles and venules were graded with twitch frequency, the fastest and largest response occurring at 6-8 Hz. Tetanic contraction, at 40 Hz for 1 s, produced faster responses in all vessels, a maximum 55% increase from resting internal diameter being attained in only 8 s in some terminal arterioles. In all vessels the responses to tetanic contraction were equal to the maximal dilatation induced by papaverine. These results, in contrast with conclusions drawn from indirect estimates of venous responses, show that venules, like arterioles, dilate actively in response to muscle contraction. Venule dilatation may reduce the rise in capillary hydrostatic pressure, thereby limiting the outward filtration of fluid.

Animals↗
PubMed1986

Microvascular pressure in venules of skeletal muscle during arterial pressure reduction.

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40-185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.

Animals↗
PubMed1999

Collagen fiber arrangement in canine hepatic venules.

Cell-maceration/scanning electron microscopy, serial sections and scanning electron microscopy of vascular resin casts were employed to demonstrate the arrangement of collagen fibers in the terminal hepatic venules, involving the central, intercalated and collecting veins in dog liver. In cell-maceration specimens, each collagen fiber was observed to run in various directions, forming a sheath with a compact meshwork of collagen fibers. The collagenous meshwork in the hepatic venules was looser than those of the terminal portal venules and hepatic arterioles. Some collagen fibers formed bundles with an elongated spiral arrangement encircling the wall of the terminal hepatic venules. In resin casts, these venules were observed as a twisted configuration caused by spiral collagen bundles. A helical modification of such connective tissue bundles might provide a mechanically stable vascular structure and permit reversible changes in linear and circumferential vascular dimensions at the terminal tributaries of veins. Round or oval pores with diameters of approximately 9 microns were also observed in the sheath of collagen fibers. These pores, together with the relatively loose collagenous meshwork in the hepatic venules, might play a role in lymphocyte migration from these venules into the surrounding tissue and provide high permeability to the venule walls. No such helical configuration and pores were observed in either the portal venules or the hepatic arterioles.

Animals↗
PubMed1999

Human conjunctiva contains high endothelial venules that express lymphocyte homing receptors.

Lymphocyte trafficking into tissues has been shown to occur across vessels with specialized endothelial cells called high endothelial venules. High endothelial venules naturally occur in lymph nodes and mucosal lymphoid tissues. The presence of high endothelial venules in the conjunctiva has not been demonstrated previously and the purpose of this study was to determine whether there is such a specialized vasculature to facilitate lymphocyte trafficking in conjunctiva associated lymphoid tissue.Samples of conjunctiva from four different individuals were analysed morphometrically for the presence of high endothelial venules by light and electron microscopy, and by immunohistochemistry using antibodies specific for high endothelial venules and for two adhesion molecules namely, Vascular Adhesion Protein-1 and Mucosal Addressin Cell Adhesion Molecule-1, expressed on high endothelial venules found in other tissues. Blood vessels with anatomical features of high endothelial venules were demonstrated in relation to conjunctival follicles and in the lamina propria. Immunohistochemical studies showed positive staining of vessels with anti-high endothelial venule antibodies, and with antibody against Vascular Adhesion Protein-1 but not with antibody against Mucosal Addressin Cell Adhesion Molecule-1. This study reveals that some of the blood vessels associated with conjunctival follicles and lamina propria have features of high endothelial venules. These vessels may play a significant role in lymphocyte homing to the conjunctiva and Vascular Adhesion Protein-1 (but not Mucosal Addressin Cell Adhesion Molecule-1) is one of the vascular addressin/adhesion molecules.

Cell Adhesion Molecules↗