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Biomedical subjects

H Li

Publications and source records attributed to H Li.

At least 631 records · Page 35Linked to original sources

Molecular characterization of the beta-N-acetylglucosaminidase of Escherichia coli and its role in cell wall recycling.

The beta-N-acetylglucosaminidase of Escherichia coli was found to have a novel specificity and to be encoded by a gene (nagZ) that maps at 25.1 min. It corresponds to an open reading frame, ycfO, whose predicted amino acid sequence is 57% identical to that of Vibrio furnissii ExoII. NagZ hydrolyzes the beta-1,4 glycosidic bond between N-acetylglucosamine and anhydro-N-acetylmuramic acid in cell wall degradation products following their importation into the cell during the process for recycling cell wall muropeptides. From amino acid sequence comparisons, the novel beta-N-acetylglucosaminidase appears to be conserved in all 12 gram-negative bacteria whose complete or partial genome sequence data are available.

Acetylglucosaminidase↗

Nitrate assimilation genes of the marine diazotrophic, filamentous cyanobacterium Trichodesmium sp. strain WH9601.

A 4.0-kb DNA fragment of Trichodesmium sp. strain WH9601 contained gene sequences encoding the nitrate reduction enzymes, nirA and narB. A third gene positioned between nirA and narB encodes a putative membrane protein with similarity to the nitrate permeases of Bacillus subtilis (NasA) and Emericella nidulans (CrnA). The gene was shown to functionally complement a DeltanasA mutant of B. subtilis and was assigned the name napA (nitrate permease). NapA was involved in both nitrate and nitrite uptake by the complemented B. subtilis cells. napA is distinct from the nrt genes that encode the nitrate transporter of freshwater cyanobacteria.

Amino Acid Sequence↗

Newly recognized herpesvirus causing malignant catarrhal fever in white-tailed deer (Odocoileus virginianus).

Malignant catarrhal fever (MCF) was diagnosed by clinical signs and lesions in five out of six white-tailed deer (Odocoileus virginianus) in a North American zoo. The clinical signs and histopathological lesions in these deer were typical of MCF. Antibody to an epitope conserved among the MCF viruses was detected in the sera collected from the deer. PCR failed to amplify viral sequences from DNA extracted from peripheral blood leukocytes (PBL) and/or spleens of the deer with primers specific for ovine herpesvirus 2 (OHV-2) or specific for alcelaphine herpesvirus 1 (AHV-1). By using degenerate primers targeting a conserved region of a herpesviral DNA polymerase gene, a DNA fragment was amplified from the PBL or spleens of all six deer and sequenced. Alignment of the sequences demonstrated that the virus in the deer belongs to the Gammaherpesvirinae subfamily, exhibiting 82% identity to OHV-2, 71% to AHV-1, and 60% to a newly identified bovine lymphotropic herpesvirus. This virus, which causes classical MCF in white-tailed deer, is a newly recognized agent belonging to the MCF group of gammaherpesviruses. It is the third reported pathogenic MCF virus, genetically distinct but closely related to OHV-2 and AHV-1. The reservoir for the virus has not been identified.

Amino Acid Sequence↗

Comparison of protein A gene sequencing with pulsed-field gel electrophoresis and epidemiologic data for molecular typing of methicillin-resistant Staphylococcus aureus.

The epidemiologic relatedness of methicillin-resistant Staphylococcus aureus (MRSA) isolates is currently determined by analysis of chromosomal DNA restriction patterns by pulsed-field gel electrophoresis (PFGE). We have evaluated an alternative typing system (MicroSeq StaphTrack Kit; Perkin-Elmer Biosystems) based on the sequence analysis of the chromosomally encoded polymorphic repeat X region of the S. aureus protein A (spa) gene. A total of 69 clinical MRSA isolates were divided into 18 groups according to the number and nucleotide sequences of the spa repeats. Molecular typing results obtained both by spa sequencing and from the PFGE patterns were concordant except for one group, which contained 20 isolates recovered over a 2-year period from hospitalized patients at the Mayo Clinic. Although the spa typing patterns were indistinguishable for those isolates, PFGE analysis yielded seven related but distinguishable patterns. Further coagulase gene sequence analysis subtyped those 20 strains into four groups which followed distinct temporal and geographic distributions. During a 2-year epidemic period there were up to 7 fragment changes in PFGE patterns among epidemiologically related isolates, suggesting that PFGE may be unsuitable for long-term typing of strains involved in epidemics. Although more limited than PFGE in discriminatory power, spa sequencing analysis could be used as a screening method for typing of MRSA strains because of the shorter turnaround time, ease of use, and the inherent advantages of sequence analysis, storage, and sharing of information.

Animals↗

Identification of coryneform bacterial isolates by ribosomal DNA sequence analysis.

Identification of coryneform bacteria to the species level is important in certain circumstances for differentiating contamination and/or colonization from infection, which influences decisions regarding clinical intervention. However, methods currently used in clinical microbiology laboratories for the species identification of coryneform bacteria are often inadequate. We evaluated the MicroSeq 500 16S bacterial sequencing kit (Perkin-Elmer Biosystems, Foster City, Calif.), which is designed to sequence the first 527 bp of the 16S rRNA gene for bacterial identification, by using 52 coryneform gram-positive bacilli from clinical specimens isolated from January through June 1993 at the Mayo Clinic. Compared to conventional and supplemented phenotypic methods, MicroSeq provided concordant results for identification to the genus level for all isolates. At the species level, MicroSeq provided concordant results for 27 of 42 (64.3%) Corynebacterium isolates and 5 of 6 (83.3%) Corynebacterium-related isolates, respectively. Within the Corynebacterium genus, MicroSeq gave identical species-level identifications for the clinically significant Corynebacterium diphtheriae (4 of 4) and Corynebacterium jeikeium (8 of 8), but it identified only 50.0% (15 of 30) of other species (P < 0.01). Four isolates from the genera Arthrobacter, Brevibacterium, and Microbacterium, which could not be identified to the species level by conventional methods, were assigned a species-level identification by MicroSeq. The total elapsed time for running a MicroSeq identification was 15.5 to 18.5 h. These data demonstrate that the MicroSeq 500 16S bacterial sequencing kit provides a potentially powerful method for the definitive identification of clinical coryneform bacterium isolates.

Actinomycetales↗

Sequestration and inhibition of Daxx-mediated transcriptional repression by PML.

PML fuses with retinoic acid receptor alpha (RARalpha) in the t(15;17) translocation that causes acute promyelocytic leukemia (APL). In addition to localizing diffusely throughout the nucleoplasm, PML mainly resides in discrete nuclear structures known as PML oncogenic domains (PODs), which are disrupted in APL and spinocellular ataxia cells. We isolated the Fas-binding protein Daxx as a PML-interacting protein in a yeast two-hybrid screen. Biochemical and immunofluorescence analyses reveal that Daxx is a nuclear protein that interacts and colocalizes with PML in the PODs. Reporter gene assay shows that Daxx drastically represses basal transcription, likely by recruiting histone deacetylases. PML, but not its oncogenic fusion PML-RARalpha, inhibits the repressor function of Daxx. In addition, SUMO-1 modification of PML is required for sequestration of Daxx to the PODs and for efficient inhibition of Daxx-mediated transcriptional repression. Consistently, Daxx is found at condensed chromatin in cells that lack PML. These data suggest that Daxx is a novel nuclear protein bearing transcriptional repressor activity that may be regulated by interaction with PML.

Adaptor Proteins, Signal Transducing↗

Metabolic regulation of Na(+)/P(i)-cotransporter-1 gene expression in H4IIE cells.

We showed that the rat Na(+)/P(i) cotransporter-1 (RNaPi-1) gene was regulated by insulin and glucose in rat hepatocytes. The aim of this work was to elucidate signaling pathways of insulin-mediated metabolic regulation of the RNaPi-1 gene in H4IIE cells. Insulin increased RNaPi-1 mRNA abundance in the presence of glucose and decreased RNaPi-1 mRNA in the absence of glucose, clearly establishing an involvement of metabolic signals for insulin-induced upregulation of the RNaPi-1 gene. Pyruvate and insulin increased RNaPi-1 expression but downregulated L-pyruvate kinase, indicating the existence of gene-specific metabolic signals. Although fructose, glycerol, and lactate could support insulin-induced upregulation of the RNaPi-1 gene, compounds entering metabolism beyond pyruvate oxidation, such as acetate and citrate, could not, suggesting that RNaPi-1-specific metabolic signals are generated at or above pyruvate oxidation. Wortmannin, LY-294002, and rapamycin abolished the insulin effect on the RNaPi-1 gene, whereas expression of dominant negative Asn(17) Ras and mitogen-activating protein kinase (MAPK) kinase (MEK) inhibitor PD-98059 exhibited no effect. Thus we herein propose that metabolic regulation of RNaPi-1 expression by insulin is mediated through the phosphatidylinositol 3-kinase/p70 ribosomal S6 kinase pathways, but not the Ras/MAPK pathway.

Adenoviridae↗

Effects of homocysteine on endothelial nitric oxide production.

Hyperhomocysteinemia (HHCy) is an independent and graded cardiovascular risk factor. HHCy is prevalent in patients with chronic renal failure, contributing to the increased mortality rate. Controversy exists as to the effects of HHCy on nitric oxide (NO) production: it has been shown that HHCy both increases and suppresses it. We addressed this problem by using amperometric electrochemical NO detection with a porphyrinic microelectrode to study responses of endothelial cells incubated with homocysteine (Hcy) to the stimulation with bradykinin, calcium ionophore, or L-arginine. Twenty-four-hour preincubation with Hcy (10, 20, and 50 microM) resulted in a gradual decline in responsiveness of endothelial cells to the above stimuli. Hcy did not affect the expression of endothelial nitric oxide synthase (eNOS), but it stimulated formation of superoxide anions, as judged by fluorescence of dichlorofluorescein, and peroxynitrite, as detected by using immunoprecipitation and immunoblotting of proteins modified by tyrosine nitration. Hcy did not directly affect the ability of recombinant eNOS to generate NO, but oxidation of sulfhydryl groups in eNOS reduced its NO-generating activity. Addition of 5-methyltetrahydrofolate restored NO responses to all agonists tested but affected neither the expression of the enzyme nor formation of nitrotyrosine-modified proteins. In addition, a scavenger of peroxynitrite or a cell-permeant superoxide dismutase mimetic reversed the Hcy-induced suppression of NO production by endothelial cells. In conclusion, electrochemical detection of NO release from cultured endothelial cells demonstrated that concentrations of Hcy >20 microM produce a significant indirect suppression of eNOS activity without any discernible effects on its expression. Folates, superoxide ions, and peroxynitrite scavengers restore the NO-generating activity to eNOS, collectively suggesting that cellular redox state plays an important role in HCy-suppressed NO-generating function of this enzyme.

Animals↗

Perfusion of the mechanically compressed lumbar ganglion with lidocaine reduces mechanical hyperalgesia and allodynia in the rat.

The rat L(5) dorsal root ganglion (DRG) was chronically compressed by inserting a hollow perforated rod into the intervertebral foramen. The DRG was constantly perfused through the hollow rod with either lidocaine or normal saline delivered by a subcutaneous osmotic pump. Behavioral evidence for neuropathic pain after DRG compression involved measuring the incidence of hindlimb withdrawals to both punctate indentations of the hind paw with mechanical probes exerting different bending forces (hyperalgesia) and to light stroking of the hind paw with a cotton wisp (tactile allodynia). Behavioral results showed that for saline-treated control rats: the withdrawal thresholds for the ipsilateral and contralateral paws to mechanical stimuli decreased significantly after surgery and the incidence of foot withdrawal to light stroking significantly increased on both ipsilateral and contralateral hind paws. Local perfusion of the compressed DRG with 2% lidocaine for 7 days at a low flow-rate (1 microl/h), or for 1 day at a high flow-rate (8 microl/h) partially reduced the decrease in the withdrawal thresholds on the ipsilateral foot but did not affect the contralateral foot. The incidence of foot withdrawal in response to light stroking with a cotton wisp decreased significantly on the ipsilateral foot and was completely abolished on the contralateral foot in the lidocaine treatment groups. This study demonstrated that compression of the L(5) DRG induced a central pain syndrome that included bilateral mechanical hyperalgesia and tactile allodynia. Results also suggest that a lidocaine block, or a reduction in abnormal activity from the compressed ganglia to the spinal cord, could partially reduce mechanical hyperalgesia and tactile allodynia.

Anesthetics, Local↗

Plasma carbon monoxide levels in term newborn infants with sepsis.

Carbon monoxide (CO) has been implicated as a new endogenously produced mediator similar to nitric oxide (NO). CO was measured in plasma samples from 7 term newborn infants with sepsis and from 30 healthy neonates. Plasma CO levels were significantly higher in the group with sepsis at the time of admission to the neonatal intensive care unit than in the healthy controls (p < 0.05). Moreover, the elevated plasma CO levels were significantly related to increased NO production, as indicated by plasma nitrite/nitrate levels (p < 0.05). The present study suggests that, in addition to NO, CO might be another important mediator taking part in the pathogenesis of neonatal sepsis.

Bacterial Infections↗

Caspase inhibitors reduce neuronal injury after focal but not global cerebral ischemia in rats.

BACKGROUND AND PURPOSE: Studies show that blocking the activation of caspases by the caspase inhibitors z-VAD.FMK and z-DEVD.FMK can reduce ischemic neuronal injury after cerebral ischemia. Because the severity of ischemia was mild in some studies, we tested the efficacy of these caspase inhibitors on moderately severe but transient forebrain and focal ischemic insults in the rat. METHODS: Various regimens of z-VAD, z-DEVD, and control DMSO were given to rats subjected to either 4-vessel occlusion ischemia (4-VO, 10-minute occlusion, 7-day survival) or distal middle cerebral artery occlusion (MCAo, 90-minute occlusion, 22.5-hour survival). In global ischemia, treatments were given immediately after ischemia (experiment 1) or as preischemic and postischemic treatments (experiment 2). Three focal ischemia experiments were done. Injection times were 60 minutes into ischemia (experiment 1) and 60 minutes into ischemia plus 30 and 120 minutes after ischemia (experiment 2). Experiment 3 was identical to experiment 2 except that a 30-minute preischemia treatment was instituted. Core normothermia was maintained in all experiments during ischemia. However, in the last focal and global experiments, core and brain temperatures, respectively, were also measured after ischemia with telemetry probes. Because hyperthermia accompanied z-DEVD treatment, an extra z-DEVD-treated group (MCAo) was included with temperature clamped at normothermia. RESULTS: Neither z-VAD nor z-DEVD significantly reduced CA1 injury after global ischemia. In focal ischemia, both drugs significantly reduced infarction, but only in the third experiment, and the prevention of hyperthermia that accompanied z-DEVD treatment did not alter this. CONCLUSIONS: These results suggest a detrimental role of caspases in moderately severe focal but not global cerebral ischemia.

Amino Acid Chloromethyl Ketones↗

Use of transcranial Doppler ultrasound to predict outcome in patients with intracranial large-artery occlusive disease.

BACKGROUND AND PURPOSE: Intracranial large-artery occlusive disease is the predominant vascular lesion found in stroke patients of Asian, African, and Hispanic ancestry, making it numerically perhaps the most common vascular cause of stroke in the world. Relatively little is known about the clinical significance of finding such lesions. We investigate whether the presence and the extent of these vascular lesions help predict outcome after stroke. METHODS: On the basis of transcranial Doppler of the intracranial arteries with supplementary duplex ultrasound of the carotid arteries, we determined the number of occlusive arteries in the craniocervical circulation of consecutive patients who were hospitalized for acute cerebral ischemia. Patients were followed for 6 months for further vascular events (including transient ischemic attack, stroke, and acute coronary syndrome) or death. RESULTS: Among 705 consecutive Chinese patients studied, occlusive arteries were found in 345 patients (49%): 258 patients (37%) had intracranial lesions only, 71 (10%) had both extracranial and intracranial lesions, and 16 (2.3%) had extracranial lesions only. Sixty-three (18%) of the 345 patients with occlusive arteries and 35 (9.7%) of the 360 patients without occlusive arteries had further vascular event or death within 6 months. The risk of vascular events or death increased rapidly with rising numbers of occlusive arteries, after adjustment for vascular risk factors and stroke severity (adjusted odds ratio [OR] 1.25 per occlusive artery, 95% CI 1.12 to 1.39). Other independent risk factors included age (OR 1.03 per year of age, 95% CI 1.01 to 1.05) and atrial fibrillation (OR 3.00, 95% CI 1.40 to 6.69). CONCLUSIONS: In patients with predominantly intracranial large-artery occlusive disease, the presence and the total number of occlusive arteries in the craniocervical circulation predict further vascular events or death within 6 months after stroke. Transcranial Doppler ultrasound is an important investigation for the evaluation of patients with stroke in populations at risk of intracranial atherosclerotic disease.

Arterial Occlusive Diseases↗

Production and interaction of oxygen and nitric oxide free radicals in PMA stimulated macrophages during the respiratory burst.

The activity of nitric oxide synthase (NOS) during the respiratory burst in phorbol-1,2-myristate-1,3-acetate (PMA) stimulated macrophages has been the topic of much debate in the literature. To help clarify the role of NOS, we have examined the chemiluminescence arising from peroxynitrite production, nitrite/nitrate and nitric oxide production, and oxygen consumption during the respiratory burst in PMA-stimulated macrophages. The Griess reaction was used to measure nitrite/nitrate, spin trapping with N-methyl D-glucamine dithiocarbamate (MGD)2-Fe2+ was used to quantify nitric oxide, and the spin probe 2,2,6,6-tetramethylpiperidine-N-oxyl-4-ol (TEMPOL) was used to measure oxygen consumption. Oxygen free radical production (hydroxyl and superoxide free radicals) was also investigated using the spin trap 5,5-dimethyl-1-pyroline-1-oxide (DMPO). The chemiluminescence emitted by the PMA-stimulated macrophages and nitrite/nitrate in the culture system were both found to increase. However, the rate of nitric oxide release remained constant, indicating that the activity of NOS is not enhanced during the respiratory burst in PMA stimulated macrophages.

Animals↗

No correlation of polymorphism of angiotensin-converting enzyme genes with left ventricular hypertrophy in essential hypertension.

To investigate the correlation of polymorphism of angiotensin-converting enzyme (ACE) genes with left ventricular hypertrophy in essential hypertension, 151 patients with essential hypertension were studied. ACE genotypes were determined by PCR technology and diastolic left ventricular diameter (DLVd), systolic left ventricular diameter (SLVd), interseptal ventricular thickness (IVS), and left ventricular posterior wall thickness (LVPW) were scanned by echocardiography. Left ventricular mass (LVM) and the left ventricular mass index (LVMI) were calculated from echocardiographic findings. Results revealed that DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the DD genotype group were 49.9 +/- 5.6 mm, 30.5 +/- 6.5 mm, 11.2 +/- 1.6 mm, 11.7 +/- 1.5 mm, 259.5 +/- 62.1 g, 92.7 +/- 23.5 g/m2, respectively. DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the ID genotype group were 8.9 +/- 5.3 mm, 31.5 +/- 5.2 mm, 11.4 +/- 1.7 mm, 11.9 +/- 1.6 mm, 261.3 +/- 70.3 g, and 94.9 +/- 25.8 g/m2, respectively, and DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the II genotype group are 48.9 +/- 5.5 mm, 31.8 +/- 6.5 mm, 11.1 +/- 1.9 mm, 11.5 +/- 1.8 mm, 250.8 +/- 82.5 g and 90.8 +/- 30.1 g/m2 respectively. There was no significant difference between the ID, DD and II genotype groups as regards DLVd, SLVd, IVS, LVPW, LVM, and LVMI (p > 0.05). These findings indicate that there is no association between the ACE gene and left ventricular hypertrophy in essential hypertension occurring in the Chinese population.

Aged↗

Role of carbon monoxide and nitric oxide in newborn infants with postasphyxial hypoxic-ischemic encephalopathy.

OBJECTIVE: To investigate the role of carbon monoxide (CO) and nitric oxide (NO) in the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). METHODS: Plasma CO and NO levels were studied in 33 asphyxiated term neonates, and 30 healthy neonates served as controls. RESULTS: Among the 33 asphyxiated term neonates, plasma CO and NO levels in 28 neonates with HIE were significantly higher than those in the 5 infants without HIE and in the normal controls. The plasma CO and NO levels in the newborn infants with HIE stage 3 were found to be significantly higher than those in the neonates with HIE stage 1 and 2. Moreover, plasma CO and NO levels were significantly increased in neonates with brain damage and adverse outcome as compared with those in patients with normal neuroimaging and normal outcome. CONCLUSION: Plasma CO and NO levels after perinatal asphyxia are related to the severity of neonatal HIE, brain damage, and neurologic outcome. The present study suggests that CO and NO might play important roles in the pathogenesis of neonatal HIE.

Asphyxia Neonatorum↗

Inverse design and CFD investigation of blood pump impeller.

In this paper, a three-dimensional inverse design method using mean swirl specification is applied to the design of centrifugal blood pump impeller blades. CFD investigation of the passage flows is carried out to analyze the flow field and pressure generated across the blade. The results show that the possibility of blood cells' damage may not be increased when the pressure developed is increased. This technique can provide designers valuable insight on the development of efficient blood pump with reduced risk of blood traumatization.

Computer Simulation↗

Consequences of a family history of type 1 and type 2 diabetes on the phenotype of patients with type 2 diabetes.

OBJECTIVE: To investigate the impact of a family history of type 1 and type 2 diabetes on the phenotype of patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: In a population-based study, we compared the phenotype in 3 groups of patients with type 2 diabetes. The first group had no family history of diabetes (FH-, n = 148); the second group had a family history of type 2 diabetes only (FH+(TYPE2), n = 1,211); and the third group had a family history of both type 1 and type 2 diabetes (FH+(MIXED), n = 240). Furthermore, we studied the frequency of GAD antibodies (GADabs), HLA-DQB1 risk genotypes, and the presence of coronary heart disease (CHD) according to family history in unrelated patients with type 2 diabetes from 787 families (148 FH-, 546 FH+(TYPE2) and 93 FH+(MIXED)). RESULTS: Patients with no family history of diabetes were older at the onset of the disease, had a better beta-cell function (P = 0.004), and had higher HDL cholesterol concentrations (P = 0.006) than patients with a family history of diabetes. Patients with a family history of only type 2 diabetes had higher BMI and fasting C-peptide concentrations (P = 0.031) but lower frequency of GADab (11 vs. 23%, P = 0.001) and DQB1 risk genotypes (37 vs. 54%, P = 0.003) compared with patients with a family history of both type 1 and type 2 diabetes. In addition, hypertension (P = 0.05) and CHD (P = 0.031) were more common in FH+(TYPE2) than in FH+(MIXED) patients. In patients <60 years old, a family history of type 1 diabetes was associated with a reduced risk of CHD independent of age, hypertension, and HDL cholesterol concentrations. The results were similar when the GADab+ patients were excluded from the analysis. CONCLUSIONS: A family history of both type 1 and type 2 diabetes had a profound influence on the phenotype of patients with type 2 diabetes, which suggests a genetic interaction between type 1 and type 2 diabetes.

Aged↗

Cell surface proteoglycan expression by human periodontal cells.

Cell surface proteoglycans are known to be involved in many functions including interactions with components of the extracellular microenvironment and serve to influence cell shape, adhesion, proliferation, and differentiation. They also can act as co-receptors, to help bind and modify the action of various growth factors and cytokines. Despite their strategic location and relevance to cell function, few studies have considered the nature of the cell surface proteoglycans associated with cells of the periodontium. Due to the structural complexity and multiplicity of cell types in the periodontium, we have selected three different cell lines (gingival connective tissue fibroblast, periodontal ligament fibroblast, and osteoblast) which each represent the unique functions within the periodontium to study the expression of cell surface proteoglycans. We hypothesized that a number of cell surface proteoglycans will be expressed by human periodontal cells and these may be related to the source and function of the cell. Western blotting and RT-PCR methods were used to study the expression of five cell surface proteoglycans (syndecan-1, -2, -4, glypican and betaglycan) in three cell lines of human periodontal cells in vitro. Our results demonstrated the expression of protein cores for syndecan-1 (43 kDa), syndecan-2 (48 kDa), syndecan-4 (35 kDa), glypican (64 kDa), and betaglycan (100-110 kDa). RT-PCR results confirmed that all of these cells produced mRNA for the cell surface proteoglycans under study, of which syndecan-2 showed a significant difference in expression between the periodontal ligament fibroblasts, gingival fibroblasts and osteoblasts. We conclude that the presence of specific cell surface proteoglycans on periodontal cells implies a likely role for these molecules in cell-cell, cell-matrix interactions involved in periodontal disease and/or regeneration of the periodontium, of which they may have distinctive functions related to the source and function of these cells.

Cell Membrane↗