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Results for “collateral cleavage”

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At least 19 recordsLinked to original sources

PubMed2026

Type IV-C CRISPR-Cas effector complexes recognize double-stranded DNA and switch on collateral cleavage of ssDNA and RNA.

Type IV-C CRISPR-Cas systems remain enigmatic compared to other class 1 systems. Here, we expand the type IV-C catalog, identifying two phylogenetically distinct clades primarily found in archaea (IV-C1) or bacteria (IV-C2), distinguishable by the Cas10IVc subunit architecture. We functionally and structurally characterize type IV-C1 systems from Thermococcus onnurineus (Ton) and Pyrococcus abyssi (Pab). Type IV-C complexes assemble with crRNAs derived from distinct CRISPR arrays and recognize a 5'-GGG-3' protospacer adjacent motif (PAM) to bind double-stranded DNA targets. Target recognition activates the HD domain of Cas10IVc, triggering metal-dependent collateral cleavage of single-stranded DNA and RNA. This behavior is explained by allosteric alignment of the HD active site, triggered by PAM-dependent R-loop formation, as revealed by cryo-EM. Together, our findings suggest that type IV-C systems provide immunity via non-specific cleavage of nucleic acids generated during mobile genetic element replication or transcription.

CP: molecular biology↗

PubMed2026

Monitoring kinetic changes and restriction of influenza A virus RNA species during infection using a Flu-Stranded CRISPR platform.

UNLABELLED: Influenza A virus (IAV) generates three closely related RNA species: viral RNA (vRNA), complementary RNA (cRNA), and messenger RNA (mRNA), whose strand-specific quantification remains limited by sensitivity and quantitative dynamic range, particularly at low RNA abundance. Here, we developed Flu-Stranded CRISPR-Cas12a, a strand-specific detection platform integrating tagged reverse transcription, segment-specific PCR, and Cas12a collateral cleavage to support quantitative analysis of all three RNA species across a broad dynamic range. The assay enables reliable detection down to 102 copies per reaction, extending the lower quantitative boundary relative to both SYBR Green and TaqMan reverse transcription quantitative PCR (RT-qPCR) under matched conditions. Validated in infected cell lines, murine lung tissues, and clinical nasopharyngeal specimens, the platform enabled subtype-discriminating, strand-resolved detection, including samples near or below the quantitative range of SYBR Green RT-qPCR. Using finely resolved infection time-course analyses in NP and NA segments, we identified a reproducible early vRNA decline within the early post-infection phase. This decline was partially attenuated in RIG-I knockout A549 cells, while subsequent vRNA accumulation was enhanced, consistent with a modulatory rather than essential role for RIG-I in early viral RNA dynamics. Subcellular fractionation localized this decline to cytoplasmic incoming genomes. In contrast, importazole-mediated inhibition of nuclear import abolished vRNA recovery without affecting the early decline, indicating that nuclear entry functionally separates early genome reduction from subsequent productive replication. These findings establish Flu-Stranded CRISPR-Cas12a as a strand-resolved framework for monitoring IAV RNA dynamics and reveal an early window of genome vulnerability during cytoplasmic transit that shapes infection outcome. IMPORTANCE: The early fate of incoming influenza virus genomes remains unclear, limiting our understanding of how infection is established or aborted in host cells. We developed Flu-Stranded CRISPR-Cas12a, a strand-specific platform for sensitive and quantitative analysis of influenza viral RNA (vRNA), complementary RNA (cRNA), and messenger RNA (mRNA) across experimental and clinical samples. Using high-resolution time-course analysis, we identified a reproducible early decline in vRNA during the post-entry phase. Our data suggest that this early genome loss arises from multiple processes, with RIG-I acting as a modulatory factor rather than a primary driver. Subcellular fractionation localized this effect to cytoplasmic incoming genomes, whereas importin-β-mediated nuclear entry was required for subsequent vRNA recovery. These findings support a model of an early cytoplasmic phase of genome attrition that is distinct from replication and provide a framework for understanding early influenza RNA kinetics and for guiding strand-resolved diagnostics and antiviral evaluation.

CRISPR-Cas12a↗

PubMed2005

Medial collateral ligament bursitis in a 12-year-old girl.

A 12-year-old female athlete, training for an international career in pentathlon, was referred to our clinic because of 2 years of recurrent localized swelling and activity-related pain in the medial aspect of her right knee, since falling from a horse and hitting her knees on the ground. She had been examined by a number of doctors over this period and treated with physiotherapy without a proper diagnosis and with no improvement. She could run only very limited distances before excruciating pain and swelling, and she had to abandon participation in competitions. During rest, the swelling decreased but never disappeared entirely. Clinical examination revealed minor effusion and localized tenderness on palpation around the medial joint line. Magnetic resonance imaging showed fluid between the medial capsule and medial collateral ligament, but could not identify any connection to the joint. Arthroscopy revealed a cleavage in the posterior medial joint capsule, superior and close to the medial meniscus, that was connected to the medial collateral ligament bursa. The cleavage was simply expanded, which emptied the bursa, followed by compression bandage and ice for 2 weeks. An immediate positive effect was observed and she could run pain free without swelling within 3 weeks of surgery. Six months after surgery, there has been no recurrence. To our knowledge, this is the first time this injury has been described in a child.

Arthroscopy↗

PubMed2001

Sonographic examination of lateral epicondylitis.

OBJECTIVE: The purpose of this study was to describe the sonographic appearance of the common extensor origin in cadavers and asymptomatic volunteers, and to relate this appearance to the findings in patients with lateral epicondylitis. SUBJECTS AND METHODS: Seventy-two elbows in 71 patients with lateral epicondylitis were examined on sonography. Most of the patients (60/71) gave a history of repetitive microtrauma. The injuries were evaluated with respect to location and severity. Focal areas of degeneration, discrete cleavage tears, and involvement of the lateral collateral ligament were identified. Calcification and bony changes were noted. The appearance of the normal common extensor tendon was described, and cadaveric specimens were dissected. Twenty-one patients subsequently underwent surgery. RESULTS: The normal common extensor origin is composed of longitudinal fibrils bound closely with the extensor carpi radialis brevis constituting most of the deep fibers, with the extensor digitorum making up the superficial part. The lateral collateral ligament can be identified as a discrete and separate band. The most common appearance of lateral epicondylitis is a focal hypoechoic area in the deep part of the tendon (46/72). These focal areas were identified at surgery and corresponded histologically to collagen degeneration with fibroblastic proliferation. Often discrete cleavage planes traversing the tendon were manifest as partial (18/72) and complete (2/72) tears. The lateral collateral ligament was involved in eight of 72 elbows. CONCLUSION: Sonography of the common extensor origin can be used to confirm lateral epicondylitis in patients with lateral elbow pain and provide information about the severity of the disease.

Adult↗

PubMed2005

Vascular endothelial growth factor C-induced collateral formation in a model of myocardial ischemia.

BACKGROUND: Besides being a known lymphangiogenic activator, vascular endothelial growth factor (VEGF)-C may express angiogenic potential by proteolytic cleavage and activation of endothelial cells. We assessed myocardial collateral formation and functional changes after adenovirus-mediated VEGF-C gene transfer in an ischemic porcine model. METHODS: Fifteen Landrace piglets underwent Ameroid-induced gradual occlusion of the left circumflex artery (LCx) and consequent progressive myocardial ischemia. Three weeks after Ameroid placement, the animals underwent gated 99mTc SPECT during rest and stress, in vivo angiography and 18FDG PET. Pigs were randomized to intramyocardial injections of adenoviruses encoding vascular endothelial growth factor (VEGF-C; n = 7) or control beta-galactosidase (LacZ; n = 5). Four weeks later, the examinations were repeated and histology was analyzed. RESULTS: Angiography showed significant progression of LCx stenosis in both groups during the treatment period. Left ventricular wall thickening (LVWT) at the LCx area in gated 99mTc SPECT remained unchanged in the VEGF-C group, indicating that VEGF-C prevented progression of myocardial ischemia, whereas LVWT deteriorated in the LacZ group (p = 0.042). Semi-quantitative assessment of 18FDG PET suggests more reduction in ischemia in the adVEGF-C group than in controls (p = 0.052). Angiography showed significant clustering of collaterals in the adVEGF-C gene transfer area compared that in LacZ (p = 0.004). von Willebrand factor staining revealed a significantly (p = 0.03) greater number of microvessels in the adVEGF-C-treated myocardium. CONCLUSIONS: This appears to be the first large-animal study in which, during progressive ischemia, functional and metabolic benefits of intramyocardial VEGF-C gene transfer were apparent. VEGF-C-induced collateral formation occurred at the site of gene transfer. The angiogenic potency of VEGF-C deserves further study as a therapeutic option.

Adenoviridae↗

PubMed2003

Post-ischemic activation of caspase-3 in the rat hippocampus: evidence of an axonal and dendritic localisation.

The relationship between caspase-3 activation and delayed neuronal death after ischemia was examined. Expression of caspase-3 was evaluated by colorimetric assay, immunoblotting and by immunohistochemistry. Apoptosis was characterised by terminal desoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labelling. Immunohistochemistry showed caspase-3 activation in the whole hippocampus as early as 30 min after ischemia with exclusive localisation in fiber systems, especially in the perforant path and mossy fibers, Schaffer-collaterals, as well as apical and basal dendrites of pyramidal cells. One day post-ischemia, the 18 kDa cleavage product of caspase-3 (p18) was seen in all cell compartments (nucleus, cytosol and dendrites) throughout the entire subfields and the dentate gyrus with high distribution in mossy fibers. Two days post-ischemia, p18 kDa was only seen in the nuclei and cytosol of hippocampal cells without specific regional differences among hippocampal subfields. A significant number of apoptotic cells appeared only in the CA1 pyramidal cells at 2-3 days post-ischemia. Our data provides the first evidence that caspase-3 activation was detectable in the trisynaptic pathway fiber bundles which probably correspond to perforant path, alvear path and collaterals of Schaffer, and that activation of caspase-3 led to execution of apoptotic cell death program in selectively vulnerable areas, but not in the resistant area of the hippocampus.

Animals↗

PubMed1985

Oscillating loop endarterectomy for peripheral vascular reconstruction.

A new technique for endarterectomy of the aorta, iliac, femoropopliteal, and three distal vessels of the lower leg is a safe and predictable method of endarterectomy that has proved to be effective. By the use of this technique the superficial femoral artery and its collateral branches are opened, considerably increasing the blood flow to the lower leg. Increased knowledge concerning thrombogenic enzymes, released when cleavage of the arterial wall is performed, has led to the use of antiplatelet and anticoagulative drug therapy. This has significantly enhanced the patency of the endarterectomized vessel. Today, with many patients having the saphenous veins harvested for coronary bypass or needing these veins for future bypass surgery, it seems reasonable to perform an endarterectomy of the femoral artery.

Arterial Occlusive Diseases↗

PubMed1996

The morphology of ligament insertions after failure at low strain velocity: an evaluation of ligament entheses in the rabbit knee.

The morphology of failed rabbit knee entheses is described after in vitro load to failure testing at low strain velocity. Avulsion fracture was the dominant failure mode both for the cruciate ligaments and the medial collateral ligament. The patellar ligament became avulsed in most cases from the patellar insertion. The ligamentous anterior attachment of the medial meniscus failed by a midsubstance rupture and the posterior fibrocartilaginous attachment by a rupture near to the meniscal horn. On histological inspection the failure characteristics usually appeared more elaborate, involving to different degrees all portions of the bone-ligament-bone complexes. Avulsion fracture through subchondral bone was often combined with a partial ligament midsubstance rupture. In few cases avulsion from the cement line was combined with a rupture between the uncalcified fibrocartilage and the ligament. The medial collateral ligament failed in one case entirely at the cement line of its femoral insertion. Horizontal rupture through the calcified fibrocartilage and a vertical cleavage crossing the tidemark were also observed. The superficial portion of the patellar ligament failed with a midsubstance rupture, and the deeper part with an avulsion through the calcified fibrocartilage or an avulsion fracture. The complex failure characteristics may be attributed to uneven loading, nonuniformity of the structure, and specific anatomical location. Subchondral bone beneath femoral and tibial insertions seems to be weaker than the transitional zone between soft tissue and hard bone at the enthesis. The overall inferior structural quality of a ruptured ligament has to be taken into account when parts of the original structure are used for suturing or reconstruction.

Animals↗

PubMed1991

Three-dimensional morphological analysis of nerve cells by scanning electron microscopy. A review.

The present review provides a rational and new approach to study the three-dimensional morphology of nerve cells in situ at both cellular and macromolecular levels, by means of conventional (SEM) and high resolution scanning electron microscopy (HRSEM). The slicing and ethanol-cryofracturing methods, the freeze-fracture SEM method and tissue preparation for HRSEM have been described. Nerve cell outer surface, axon hillock and initial axon segment, axonal collateral ramifications and dendritic processes were visualized either by the slicing technique or the cryofracture method displaying neuronal geometry in situ. The cleavage plane occurred at the satellite neuroglial sheath exposing somatic hidden surfaces synaptic morphology. "En passant" axospinodendritic junctions, glomerular synapses and axosomatic contacts were examined in vertebrate cerebellar cortex. The SEM and cryofracture techniques could be applied as the Golgi light microscope technique to trace short neuronal circuits. The nerve cell inner surfaces were also studied by means of freeze-fracture SEM method and HRSEM. HRSEM provided information at both cellular and macromolecular levels. Topographic contrast of glycocalyx-like substance, synaptic junctions and myelin sheath was obtained. A comparison could be made between Au/Pd and chromium coated nerve cells. HRSEM provided SE-1 images of lipoprotein domains at the myelin sheath and globular subunits at the level of the postsynaptic membrane. This latter observation offers new potential areas for future studies on receptor morphology.

Animals↗

PubMed1999

Reg1ulatory role and molecular interactions of a cell-surface heparan sulfate proteoglycan (N-syndecan) in hippocampal long-term potentiation.

The cellular mechanisms responsible for synaptic plasticity involve interactions between neurons and the extracellular matrix. Heparan sulfates (HSs) constitute a group of glycosaminoglycans that accumulate in the beta-amyloid deposits in Alzheimer's disease and influence the development of neuron-target contacts by interacting with other cell surface and matrix molecules. However, the contribution of HSs to brain function is unknown. We found that HSs play a crucial role in long-term potentiation (LTP), a finding that is consistent with the idea that converging molecular mechanisms are used in the development of neuron-target contacts and in activity-induced synaptic plasticity in adults. Enzymatic cleavage of HS by heparitinase as well as addition of soluble heparin-type carbohydrates prevented expression of LTP in response to 100 Hz/1 sec stimulation of Schaffer collaterals in rat hippocampal slices. A prominent carrier protein for the type of glycans implicated in LTP regulation in the adult hippocampus was identified as N-syndecan (syndecan-3), a transmembrane proteoglycan that was expressed at the processes of the CA1 pyramidal neurons in an activity-dependent manner. Addition of soluble N-syndecan into the CA1 dendritic area prevented tetanus-induced LTP. A major substrate of src-type kinases, cortactin (p80/85), and the tyrosine kinase fyn copurified with N-syndecan from hippocampus. Moreover, association of both cortactin and fyn to N-syndecan was rapidly increased after induction of LTP. N-syndecan may thus act as an important regulator in the activity-dependent modulation of neuronal connectivity by transmitting signals between extracellular heparin-binding factors and the fyn signaling pathway.

Animals↗

PubMed2003

Activation of the c-Jun N-terminal kinase signaling cascade mediates the effect of amyloid-beta on long term potentiation and cell death in hippocampus: a role for interleukin-1beta?

Amyloid-beta (Abeta) is a major constituent of the neuritic plaque found in the brain of Alzheimer's disease patients, and a great deal of evidence suggests that the neuronal loss that is associated with the disease is a consequence of the actions of Abeta. In the past few years, it has become apparent that activation of c-Jun N-terminal kinase (JNK) mediates some of the effects of Abeta on cultured cells; in particular, the evidence suggests that Abeta-triggered JNK activation leads to cell death. In this study, we investigated the effect of intracerebroventricular injection of Abeta(1-40) on signaling events in the hippocampus and on long term potentiation in Schaffer collateral CA1 pyramidal cell synapses in vivo. We report that Abeta(1-40) induced activation of JNK in CA1 and that this was coupled with expression of the proapoptotic protein, Bax, cytosolic cytochrome c, poly-(ADP-ribose) polymerase cleavage, and Fas ligand expression in the hippocampus. These data indicate that Abeta(1-40) inhibited expression of long term potentiation, and this effect was abrogated by administration of the JNK inhibitor peptide, D-JNKI1. In parallel with these findings, we observed that Abeta-induced changes in caspase-3 activation and TdT-mediated dUTP nick-end labeling staining in neuronal cultured cells were inhibited by D-JNKI1. We present evidence suggesting that interleukin (IL)-1beta plays a significant role in mediating the effects of Abeta(1-40) because Abeta(1-40) increased hippocampal IL-1beta and because several effects of Abeta(1-40) were inhibited by the caspase-1 inhibitor Ac-YVAD-CMK. On the basis of our findings, we propose that Abeta-induced changes in hippocampal plasticity are likely to be dependent upon IL-1beta-triggered activation of JNK.

Amyloid beta-Peptides↗

PubMed2003

Modified radical inguinal lymphadenectomy for carcinoma of the penis: technique and results.

PURPOSE: Modified radical inguinal lymphadenectomy for carcinoma of the penis is presented that satisfies the requirement for complete groin dissection, while significantly decreasing postoperative complications. MATERIALS AND METHODS: Eight patients with squamous cell carcinoma and 2 with leiomyosarcoma of the penis underwent bilateral modified inguinal lymphadenectomy, including removal of the superficial and deep inguinal lymph nodes. To avoid damage to the vessels of the groin region that run parallel to the inguinal ligament and lie in the fat of the superficial layer of the superficial fascia dissection is done beneath this layer. The proper cleavage plane is just above the membranous layer of the superficial fascia, beneath which the superficial inguinal lymph nodes are located. The saphenous vein is preserved and the sartorius muscle is left in situ, so as not to disturb collateral lymphatic drainage. RESULTS: At a followup of 6 to 104 months no skin necrosis, infection or deep venous thrombosis occurred. In 2 patients early moderate lymphedema of the lower extremities resolved with time, 2 had scrotal edema and 3 had a transient lymphocele. CONCLUSIONS: As described, modified radical inguinal lymphadenectomy decreases the morbidity associated with groin dissection, while removing superficial and deep inguinal lymph nodes.

Adult↗

PubMedDate not supplied

Role of Slit proteins in the vertebrate brain.

Diffusible chemorepellents play a major role in guiding developing axons towards their correct targets by preventing them from entering or steering them away from certain regions. Genetic studies in Drosophila revealed a novel repulsive guidance system that prevents inappropriate axons from crossing the CNS midline; this repulsive system is mediated by the Roundabout (Robo) receptors and their secreted ligand Slits. Three distinct slit genes (slit1, slit2 and slit3) and three distinct robo genes (robo1, robo2 and rig-1) have been cloned in mammals. In collagen gel co-cultures, Slit1 and Slit2 can repel and collapse olfactory axons. However, there is also some positive effect associated with Slits, as Slit2 stimulates the formation of axon collateral branches by NGF-responsive neurons of the dorsal root ganglia (DRG). Slit2 is a large ECM glycoproteins of about 200 kD, which is proteolytically processed into 140 kD N-terminal and 55-60 kD C-terminal fragments. Slit2 cleavage fragments appear to have different cell association characteristics, with the smaller C-terminal fragment being more diffusible and the larger N-terminal and uncleaved fragments being more tightly cell associated. This suggested that the different fragments might have different functional activities in vivo. We have begun to explore these questions by engineering mutant and truncated versions of hSlit2 representing the two cleavage fragments, N- and C-, and the uncleavable molecule and examining the activities of these mutants in binding and functional assays. We found that an axon's response to Slit2 is not absolute, but rather is reflective of the context in which the protein is encountered.

Animals↗

PubMed1996

Catabolism and loss of proteoglycans from cultures of bovine collateral ligament.

This paper investigates the kinetics and mechanism of loss of the two major proteoglycan species from cultures of bovine collateral ligament. Following incubation of ligament with [35S]sulfate after 6 days in culture, the rate of loss of the predominant proteoglycan species, decorin, from the matrix was shown to be much slower (t1/2 approximately 18 days) than that of the large chondroitin sulfate proteoglycan (t1/2 approximately 1.4 days). Analysis of 35S-labeled proteoglycans released into the medium between Days 11 and 15 of the culture period on a column of Sepharose CL-4B revealed that these macromolecules constituted mainly decorin of similar hydrodynamic size to that present in the matrix. Furthermore, analysis of core proteins using gel electrophoresis followed by fluorography or immunodetection with LF-94, an antibody directed against the amino-terminal region of decorin, indicated that the core proteins of decorin released into the medium and those remaining in the matrix of ligament cultures had a similar molecular mass (approximately 49 kDa). Analysis of both the 35S-labeled and endogenous macromolecules using 5/6/3-B-3, an antibody directed against terminal unsaturated chondroitin-6-sulfate disaccharides, revealed that three core proteins with molecular masses greater than approximately 200 kDa were present in the matrix. Four additional core proteins (range approximately 80-200 kDa) derived from the large proteoglycan were detected in the medium of ligament cultures. These findings indicate that, unlike decorin, the loss of the large chondroitin sulfate proteoglycan from the matrix of ligament cultures involved proteolytic cleavage of its core protein. No difference in the hydrodynamic size of the 35S-labeled glycosaminoglycan chains derived from either proteoglycan species remaining in the matrix or released into the medium of ligament cultures was observed.

Animals↗

PubMed2001

Semiquantitative analysis of types I and III collagen from tendons and ligaments in a rabbit model.

The present study presents a simple and reliable micro-method for the semiquantitative analysis of types I and III collagen in tendons and ligaments in a rabbit model. After pretreatment of the analytical material by homogenization, a double cyanogen bromide cleavage was performed and the peptide fragments were visualized by polyacrylamide gel electrophoresis and silvcr staining. On the basis of this procedure, the method presented here can be used to analyze very small amounts of sample material (less than 10microg) by electrophoresis. The results of the study showed that type I collagen is predominant in the ligaments and the tendons of the knee, e.g., medial and lateral collateral ligaments. anterior and posterior cruciate ligaments. patellar tendon, achilles tendon, and semitendinosus tendon. However, a markedly higher proportion of type III collagen was detected in the ligaments (approximately 10%) than in the tendons (approximately 5%). The ligaments differ markedly from the tendons in biochemical mapping; the ligaments are functionally and metabolically the more active tissue and have a higher adaptation potential.

Animals↗

PubMed2006

Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization.

Cardiac failure has a principal underlying aetiology of ischaemic damage arising from vascular insufficiency. Molecules that regulate collateral growth in the ischaemic heart also regulate coronary vasculature formation during embryogenesis. Here we identify thymosin beta4 (Tbeta4) as essential for all aspects of coronary vessel development in mice, and demonstrate that Tbeta4 stimulates significant outgrowth from quiescent adult epicardial explants, restoring pluripotency and triggering differentiation of fibroblasts, smooth muscle cells and endothelial cells. Tbeta4 knockdown in the heart is accompanied by significant reduction in the pro-angiogenic cleavage product N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). Although injection of AcSDKP was unable to rescue Tbeta4 mutant hearts, it significantly enhanced endothelial cell differentiation from adult epicardially derived precursor cells. This study identifies Tbeta4 and AcSDKP as potent stimulators of coronary vasculogenesis and angiogenesis, and reveals Tbeta4-induced adult epicardial cells as a viable source of vascular progenitors for continued renewal of regressed vessels at low basal level or sustained neovascularization following cardiac injury.

Animals↗

PubMed1988

In vitro nerve-growth-promoting activity of human plasma alpha 1-acid glycoprotein.

Human plasma alpha 1-acid glycoprotein or orosomucoid (OR), and its derivatives, prepared by sequential enzymatic cleavage of the carbohydrate units, were tested for their nerve-growth-promoting activities with explants of whole dorsal root ganglia from chick embryos. The results showed that the OR derivatives with terminal galactose, N-acetylglucosamine, or mannose have marked neurite-promoting activities. These preparations at a concentration of 100 micrograms/ml are equivalent to 5% fetal bovine serum (protein concentration 3,000 micrograms/ml) in their ability to elicit extensive neurite outgrowth and collateral branching. The asialo-OR, or ASOR, is the most potent form: its activity is estimated to be 20 times higher than that of transferrin and 100 times over that of fibronectin; it is approximately 1/1,500 that of NGF. The neurite-promoting activity of OR is independent of the non-neuronal cells and their products and can be blocked by a specific antiserum against OR. The mode of action of OR on the in vitro nerve growth is discussed and the pathophysiological significance of this plasma glycoprotein is considered in light of data from recent clinical and pathological studies.

Animals↗

PubMed2005

Proteoglycans and catabolic products of proteoglycans present in ligament.

The aim of the present study was to characterize the proteoglycans and catabolic products of proteoglycans present in the tensile region of ligament and explant cultures of this tissue, and to compare these with those observed in the tensile region of tendon. Approx. 90% of the total proteoglycans in fresh ligament was decorin, as estimated by N-terminal amino acid sequence analysis. Other species that were detected were biglycan and the large proteoglycans versican (splice variants V(0) and/or V1 and/or V2) and aggrecan. Approx. 23% of decorin detected in the matrix was degraded. Intact decorin and decorin fragments similar to those observed in the matrix that retained the N-terminus were also observed in the medium of ligament cultures. Intact biglycan core protein was detected in the matrix and medium of ligament cultures, and two fragments originating from the N-terminal region of biglycan were observed in the matrix of cultured ligament. Versican and versican fragments that retained the N-terminus of versican core protein were detected in fresh matrix and medium of tendon cultures. Approx. 42% of versican present in the fresh ligament was degraded. Aggrecan catabolites appearing in the culture medium were derived from aggrecanase cleavage of the core protein. An intact link protein and a degradation product from the N-terminal region of type XII collagen were also detected in the medium of the ligament explant.

Aggrecans↗