scholarly journals Assessment of Control Tissue for Gene and Protein Expression Studies: A Comparison of Three Alternative Lung Sources

2012 ◽  
Vol 2012 ◽  
pp. 1-8
Author(s):  
Margaret R. Passmore ◽  
Maria Nataatmadja ◽  
John F. Fraser
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Matrix Metalloproteinase 2 ◽  
Control Group ◽  
Expression Levels ◽  
Matrix Metalloproteinase 1 ◽  
Expression Studies ◽  
Gene And Protein Expression

The use of an appropriate control group in human research is essential in investigating the level of a pathological disorder. This study aimed to compare three alternative sources of control lung tissue and to determine their suitability for gene and protein expression studies. Gene and protein expression levels of the vascular endothelial growth factor (VEGF) and gelatinase families and their receptors were measured using real-time reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. The gene expression levels of VEGFA, placental growth factor (PGF), and their receptors, fms-related tyrosine kinase 1 (FLT1), and kinase insert domain receptor (KDR) as well as matrix metalloproteinase-2 (MMP-2) and the inhibitors, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and TIMP-2 were significantly higher in lung cancer resections. The gene expression level of MMP-9 was significantly lower in the corresponding samples. Altered protein expression was also detected, depending on the area assessed. The results of this study show that none of the three control groups studied are completely suitable for gene and protein studies associated with the VEGF and gelatinase families, highlighting the need for researchers to be selective in which controls they opt for.

Expression of Vascular Endothelial Growth Factor, Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 in Polycystic Ovarian Syndrome Rats and Its Implication

2021 ◽  
Vol 11 (5) ◽  
pp. 841-846
Author(s):  
Wei Li ◽  
Yufang Zhang ◽  
Fuping Li ◽  
Yufen Shi ◽  
Yan Wang
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Matrix Metalloproteinase 2 ◽  
Control Group ◽  
Vaginal Smear ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Polycystic ovary syndrome (PCOS) is a female endocrine disorder and frequently leads to infertility. Vascular endothelial growth factor (VEGF) has crucial roles and matrix metalloproteinase (MMPs) is correlated with cell migration. Both of them are involved in the occurrence and progression of PCOS. This study established a rat PCOS model using letrozole to measure the expression of VEGF, MMP-2 and MMP-9 (MMP-2/9), to analyze its correlation with PCOS. Letrozole was applied by gavage to establish rat PCOS model. General condition and ovarian tissue morphology were observed under a light field microscope. ELISA and immunohistochemistry (IHC) were used to detect serum or tissue expression of VEGF, MMP-2/9. Estrous cycle of rats was disrupted after 12 d for using letrozole. Vaginal smear showed abundant leukocytes with sparse keratinocytes. Ovary showed whitening and increased volume, with early phase small follicles plus lower granular cells or corpus luteum. Compared to control group, experimental group had significantly higher VEGF, MMP-2/9 (P < 0.05), which were higher in antral follicles than those in preantral follicle with higher expressions than primordial follicle (P < 0.05). In conclusion, VEGF, MMP-2/9 are abundantly expressed in both serum and tissues of PCOS rats.

scholarly journals Nitrergic neuromuscular transmission in the mouse internal anal sphincter is accomplished by multiple pathways and postjunctional effector cells

2014 ◽  
Vol 307 (11) ◽  
pp. G1057-G1072 ◽  
Author(s):  
C. A. Cobine ◽  
A. G. Sotherton ◽  
L. E. Peri ◽  
K. M. Sanders ◽  
S. M. Ward ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Anal Sphincter ◽  
Internal Anal Sphincter ◽  
Neuromuscular Transmission ◽  
Second Messengers ◽  
Cell Types ◽  
Effector Cells ◽  
Expression Levels ◽  
Gene And Protein Expression

The effector cells and second messengers participating in nitrergic neuromuscular transmission (NMT) were investigated in the mouse internal anal sphincter (IAS). Protein expression of guanylate cyclase (GCα, GCβ) and cyclic GMP-dependent protein kinase I (cGKI) were examined in cryostat sections with dual-labeling immunohistochemical techniques in PDGFRα+ cells, interstitial cells of Cajal (ICC), and smooth muscle cells (SMC). Gene expression levels were determined with quantitative PCR of dispersed cells from Pdgfrα egfp/+, Kit copGFP/+, and smMHC Cre-egfp mice sorted with FACS. The relative gene and protein expression levels of GCα and GCβ were PDGFRα+ cells > ICC ≫ SMC. In contrast, cGKI gene expression sequence was SMC = ICC > PDGFRα+ cells whereas cGKI protein expression sequence was neurons > SMC ≫ ICC = PDGFRα+ cells. The functional role of cGKI was investigated in cGKI −/− mice. Relaxation with 8-bromo (8-Br)-cGMP was greatly reduced in cGKI −/− mice whereas responses to sodium nitroprusside (SNP) were partially reduced and forskolin responses were unchanged. A nitrergic relaxation occurred with nerve stimulation (NS, 5 Hz, 60 s) in cGKI +/+ and cGKI −/− mice although there was a small reduction in the cGKI −/− mouse. Nω-nitro-l-arginine (l-NNA) abolished responses during the first 20–30 s of NS in both animals. The GC inhibitor ODQ greatly reduced or abolished SNP and nitrergic NS responses in both animals. These data confirm an essential role for GC in NO-induced relaxation in the IAS. However, the expression of GC and cGKI by all three cell types suggests that each may participate in coordinating muscular responses to NO. The persistence of nitrergic NMT in the cGKI −/− mouse suggests the presence of a significant GC-dependent, cGKI-independent pathway.

scholarly journals Expression levels of MCP-1, HGF, and IGF-1 in endometriotic patients compared with non-endometriotic controls

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sahel Heidari ◽  
Roya Kolahdouz-Mohammadi ◽  
Sepideh Khodaverdi ◽  
Nader Tajik ◽  
Ali-Akbar Delbandi
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Protein Expression ◽  
Mononuclear Cells ◽  
Endometrial Stromal Cells ◽  
Peripheral Blood Mononuclear ◽  
Monocyte Chemoattractant Protein 1 ◽  
Gene And Protein Expression ◽  
Its Gene ◽  
Hepatocyte Growth

Abstract Background To study the concentrations of monocyte chemoattractant protein-1 (MCP-1), hepatocyte growth factor (HGF), and insulin-like growth factor-1 (IGF-1) in peritoneal fluid (PF) and serum, and to evaluate their expressions by PF and peripheral blood mononuclear cells (PFMCs and PBMCs, respectively), and ectopic and eutopic endometrial stromal cells of patients with endometriosis (EESCs and EuESCs, respectively) compared with controls. Methods The concentrations of mentioned cytokines in serum and PF, as well as their expression in PBMCs, PFMCs, EuESCs and EESCs from endometriosis patients and controls were assessed. Results The levels of MCP-1, HGF, and IGF-1 in serum and PF in women with endometriosis were significantly higher than the controls (P < 0.05–P < 0.001). Gene expression of MCP-1 and IGF-1 in the PFMCs, PBMCs and EESCs also showed an increased level compared to controls (P < 0.05–P < 0.01). The protein expression of MCP-1 and IGF-1 by PFMCs was statistically higher in endometriotic women (P < 0.05 and P < 0.01, respectively). The gene and protein expression of HGF in PFMCs and its gene expression by EESCs were significantly higher in endometriotic women compared to controls (P < 0.05–P < 0.01). Conclusions The higher concentrations of mentioned cytokines in serum and PF and their higher expression by PFMCs and EESCs in endometriosis patients may contribute to the development of endometriosis.

Inducible Levels of Gelatinase B/Matrix Metalloproteinase-9 Gene Expression in Monocytes Are Associated with Marrow Cellularity in Myelodysplastic Syndrome (MDS).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1391-1391
Author(s):  
Mineo Iwata ◽  
Manoj Pillai ◽  
H. Joachim Deeg ◽  
Ghislain Opdenakker ◽  
Beverly Torok-Storb
Keyword(s):  
Gene Expression ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Myelodysplastic Syndrome ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Matrix Metalloproteinase 9 ◽  
Gene And Protein Expression ◽  
Marrow Cellularity ◽  
Metalloproteinase 9

Abstract Evidence suggests that within the hematopoietic microenvironment (ME) stromal cell function can be modified by activities produced by monocytes/macrophages and that the reciprocal is also true; stroma can influence monocyte function. Critical regulatory molecules produced by stroma are often membrane bound until cleaved by metalloproteinases (MMP); cleavage can serve to either activate or inactivate their functions, making MMPs critical components of hematopoietic regulation. We report here that gene and protein expression of human matrix metalloproteinase-9 (MMP-9) is induced in monocytes in vitro by stromal cell conditioned media (CM). Briefly, flow sorted CD14+ peripheral blood monocytes were cultured for 5 days in the presence or absence of CM from HS-5 stromal cells, and MMP-9 gene expression was determined by real time PCR. Little or no MMP-9 gene expression was detected in CD14+ cells on day 0 prior to culture. In contrast, after 5 days of culture in control media MMP-9 gene expression was increased significantly (p=0.02). However culturing CD14+ cells in CM significantly increased expression another 3 fold (p&lt;0.0001). MMP-9 protein secretion was also increased 12-fold after culture in CM. To identify which factors participate in the induction of MMP-9, the levels of MMP-9 mRNA were determined after CD14+ cells were cultured for 5 days in the presence or absence of 9 different recombinant factors. Factors chosen were those known to be present in CM and known to have their receptors expressed by monocytes. MMP-9 gene and protein expression increased 4 to 8-fold with 0.5ng/mL MCP-1/CCL2 or IL-1b, other factors tested had negligible effects. Immune cytochemical localization of MMP-9 protein in bone marrow biopsies from healthy donors and patients with myelodysplastic syndrome (MDS) indicated that mature myeloid cells including granulocytes and monocytes were stained strongly for MMP-9 protein, whereas stromal cells, fat cells, megakaryocytes, immature myeloid cells, blasts and cells of the erythroid lineage were negative. While levels of CM-induced MMP-9 gene expression among monocytes from 10 normal donors were relatively consistent, there was significant variation in inducible gene expression among CD14+ cells from 25 MDS patients (p= 0.02). Further analysis of MMP-9 gene expression in MDS mononuclear cells indicated that induced levels were negatively correlated with the degree of marrow cellularity (p=0.0002). Although marrow cellularity is a subjective estimate that can vary from one area of bone to another, the strong statistical correlation obtained suggests it may be related directly or indirectly to MMP-9 levels. In conclusion, monocytes can express and secrete MMP-9 in response to factors secreted by stromal cells. We hypothesize that the response of MDS monocytes to stromal signals can be abnormal resulting in unusually high or low levels of MMP-9, and that this may, directly or indirectly, influence marrow cellularity in MDS patients.

Thrombospondin-1 (TSP1) Promotes Thrombin Generation on the Surface of Fibroblasts (HS-68) and Induces Up-Regulation of Connective Tissue Growth Factor (CTGF) Gene and Protein Expression.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1755-1755 ◽  
Author(s):  
Joanne Manns ◽  
Mario Rico ◽  
Leonard L. Mason ◽  
De La Cadena A. Raul
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Protein Expression ◽  
Thrombin Generation ◽  
Human Fibroblasts ◽  
Inhibitory Effect ◽  
Factor V ◽  
Prothrombinase Complex ◽  
Gene And Protein Expression

Abstract TSP1 has the ability to bind to human fibroblasts, to form a complex with coagulation factor V/Va (Thrombosis Research 116:533, 2005), to promote thrombin generation on the surface of a monocytic cell line and to neutralize tissue factor pathway inhibitor (TFPI) (J Biol Chem275:31715, 2000). Disruption of TSP1 binding to neutrophils was associated with beneficial effects in an experimental animal model of inflammation, in part, by down regulating CTGF gene and protein expression (Arthritis Rheum54:2415, 2006). CTGF is a novel potent cysteine-rich heparin-binding growth factor and is highly expressed by fibroblasts. CTGF plays a major role in angiogenesis and fibrosis. There is also growing evidence that CTGF may be the downstream autocrine mediator responsible for some of the cellular effects of TGF-beta. Since fibroblasts express tissue factor (TF) on their surface, and purified thrombin and TF-VIIa complex have been shown to up-regulate the gene expression of CTGF (J Biol Chem275:14632, 2000) experiments were conducted to evaluate the ability of HS-68 to support assembly of the prothrombinase complex, TF-FVIIa, thrombin generation and the effect of thrombin generation on CTGF expression. The role of TSP1 in these reactions was assessed as well. Thrombin generation was measured by the chromogenic substrate S-2238. Although the initial rates of the reactions are available we are presenting the end-point values of the reaction expressed in umol/L of pNA released per minute. All reaction mixtures were performed in the presence of 2mM Ca++. When HS-68 cells were preincubated with FVII (5 nM) prior to the addition of activated factor V (FVa, 45nM)), FX (5nM) and prothrombin (FII, 1.4 uM), thrombin was efficiently generated (282 umol/L pNA/min), indicating that FVII was activated by TF expressed by the cell and that the HS-68 cell membrane provided an ideal surface for the reaction to occur. The addition of FII, FV, FVII and FX to the reaction mixtures was an absolute requirement. When the reaction mixture was evaluated in the presence of FII, FV, FVII, FX and TFPI (8nM), there was a 70% reduction in thrombin production (86 umol/L pNA released) confirming the important role of TFPI in regulating the activity of the TF-FVIIa complex. The addition of TSP1 to the reaction mixture containing FII, FV, FVII and FX at concentrations found in plasma during the inflammatory response (20nM) enhanced the production of thrombin (327 umol/L pNA released per min) and neutralized the inhibitory effect of TFPI by 50% (171 umol/L pNA released per min). Therefore, TSP1 promotes thrombin generation by participating in the assembly of the prothrombinase complex on the surface of HS-68 cells and by neutralizing, in part, the inhibitory effect of TFPI on TF-VIIa complex. Finally, thrombin generation on the surface of HS-68 cells was associated with up-regulation of CTGF gene expression from the baseline value by 67% at 1hr and 72% by 2 hrs. In summary, we have identified on human fibroblasts a pathway previously shown to play an important role on human neutrophils and in an experimental model of inflammation. Our laboratory is currently characterizing the binding of TSP1 to this cell line and silencing the gene for TSP1 to test its potential therapeutic benefit in an experimental model of erosive arthritis and to further determine the role of TSP1 in this pathway.

scholarly journals TRPV Subfamily (TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6) Gene and Protein Expression in Patients with Ulcerative Colitis

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Joel J. Toledo Mauriño ◽  
Gabriela Fonseca-Camarillo ◽  
Janette Furuzawa-Carballeda ◽  
Rafael Barreto-Zuñiga ◽  
Braulio Martínez Benítez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ulcerative Colitis ◽  
Protein Expression ◽  
Gastrointestinal Diseases ◽  
Control Group ◽  
Mrna Levels ◽  
Colonic Tissue ◽  
Formalin Fixed Paraffin ◽  
Gene And Protein Expression ◽  
Formalin Fixed Paraffin Embedded

Introduction. TRPVs are a group of receptors with a channel activity predominantly permeable to Ca2+. This subfamily is involved in the development of gastrointestinal diseases such as ulcerative colitis (UC). The aim of the study was to characterize the gene and protein expression of the TRPV subfamily in UC patients and controls. Methods. We determined by quantitative PCR the gene expression of TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6 in 45 UC patients (29 active UC and 16 remission UC) and 26 noninflamed controls. Protein expression was evaluated in 5 μm thick sections of formalin-fixed, paraffin-embedded tissue from 5 customized severe active UC patients and 5 control surgical specimens. Results. TRPV2 gene expression was increased in the control group compared with active UC and remission patients (P=0.002 and P=0.05, respectively). TRPV3 gene expression was significantly higher in controls than in active UC patients (P=0.002). The gene expression of TRPV4 was significantly higher in colonic tissue from patients with remission UC compared with active UC patients (P=0.05) and controls (P=0.005). TRPV5 had significantly higher mRNA levels in a control group compared with active UC patients (P=0.02). The gene expression of TRPV6 was significantly higher in the colonic tissue from patients with active UC compared with the control group (P=0.05). The protein expression of TRPV2 was upregulated in the mucosa and submucosa from the controls compared with the UC patients (P≤0.003). The protein expression of TRPV3 and TRPV4 was upregulated in all intestinal layers from the controls compared with the UC patients (P<0.001). TRPV5 was upregulated in the submucosa and serosa from the controls vs. UC patients (P<0.001). TRPV6 was upregulated in all intestinal layers from the UC patients vs. controls (P≤0.001). Conclusion. The TRPV subfamily clearly showed a differential expression in the UC patients compared with the controls, suggesting their role in the pathophysiology of UC.

Expression of iron-related proteins in the duodenum is up-regulated in patients with chronic inflammatory disorders

2013 ◽  
Vol 111 (6) ◽  
pp. 1059-1068 ◽  
Author(s):  
Abitha Sukumaran ◽  
Jithu James ◽  
Harish Palleti Janardhan ◽  
Anita Amaladas ◽  
Lekshmy Madathilazhikathu Suresh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Control Group ◽  
Divalent Metal Transporter 1 ◽  
Divalent Metal Transporter ◽  
Inflammatory Disorders ◽  
Inflammatory Conditions ◽  
Gene And Protein Expression ◽  
Fe Homeostasis ◽  
Related Proteins

Mechanisms responsible for derangements in Fe homeostasis in chronic inflammatory conditions are not entirely clear. The aim of the present study was to test the hypothesis that inflammation affects the expression of Fe-related proteins in the duodenum and monocytes of patients with chronic inflammatory disorders, thus contributing to dysregulated Fe homeostasis. Duodenal mucosal samples and peripheral blood monocytes obtained from patients with chronic inflammatory disorders, namely ulcerative colitis (UC), Crohn's disease (CD) and rheumatoid arthritis, were used for gene and protein expression studies. Hb levels were significantly lower and serum C-reactive protein levels were significantly higher in patients in the disease groups. The gene expression of several Fe-related proteins in the duodenum was significantly up-regulated in patients with UC and CD. In patients with UC, the protein expression of divalent metal transporter 1 and ferroportin, which are involved in the absorption of dietary non-haem Fe, was also found to be significantly higher in the duodenal mucosa. The gene expression of the duodenal proteins of interest correlated positively with one another and negatively with Hb. In patients with UC, the gene expression of Fe-related proteins in monocytes was found to be unaffected. In a separate group of patients with UC, serum hepcidin levels were found to be significantly lower than those in the control group. In conclusion, the expression of Fe-related proteins was up-regulated in the duodenum of patients with chronic inflammatory conditions in the present study. The effects appeared to be secondary to anaemia and the consequent erythropoietic drive.

Spatiotemporal expression profile of proteases and immunological, angiogenic, hormonal and apoptotic mediators in rat placenta before and during intrauterine trophoblast migration

2017 ◽  
Vol 29 (9) ◽  
pp. 1774 ◽  
Author(s):  
Juneo F. Silva ◽  
Natália M. Ocarino ◽  
Rogéria Serakides
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Growth Factor ◽  
Nitric Oxide Synthase ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Trophoblast Invasion ◽  
Toll Like Receptor ◽  
Oxide Synthase ◽  
Trophoblast Migration

The gene and/or protein expression of proteases and immunological, angiogenic, hormonal and apoptotic mediators was evaluated in rat placenta before and during intrauterine trophoblast migration. The depth of interstitial and endovascular intrauterine trophoblast invasion and the immunohistochemical expression of vascular endothelial growth factor (VEGF), fetal liver kinase 1 (Flk1), interferon (IFN)-γ, migration inhibitory factor (MIF), and inducible nitric oxide synthase (iNOS; also known as nitric oxide synthase (NOS) 2) were evaluated. In addition, the expression of the Vegf, Flk1, placental growth factor (Pigf), soluble fms-like tyrosine kinase 1 (sFlt1), placental lactogen 1 (Pl1), proliferin-related protein (rPlf), placental leptin (Lep), Toll-like receptor 2 (Tlr2), Toll-like receptor 4 (Tlr4), Infg, Mif, tumour necrosis factor-α (Tnf), interleukin-10 (Il10), Nos2, caspase 3 (Casp3), Bax, Bcl2, matrix metalloproteinase 2 (Mmp2) and matrix metalloproteinase 9 (Mmp9) genes was determined by real-time reverse transcription–polymerase chain reaction. At 10 days gestation, gene expression of Tlr2, Tlr4, Tnf, Infg, Il10, Casp3, Pigf, sFlt1 and Lep (P < 0.05) were higher than at 14 and/or 19 days of gestation. The beginning of intrauterine trophoblast invasion, i.e., at 14 days of gestation, coincided with higher gene and/or protein expression of MMP9, VEGF, Flk1, NOS2, MIF, BAX and rPlf compared to days 10 and 19 (P < 0.05). In contrast, gene expression of Mmp2 and Pl1 was higher at the end of trophoblast invasion compared to 10 and 14 days of gestation (P < 0.05). In conclusion, before intrauterine trophoblast migration, expression of TLRs and immunological and pro-apoptotic mediators is higher, whereas the beginning of trophoblast migration is characterised by higher expression of the pro-angiogenic factors NOS2 and MMP9. In contrast, MMP2 and PL1 expression is higher at the end of intrauterine trophoblast migration.

Temporal extracellular matrix adaptations in ligament during wound healing and hindlimb unloading

2007 ◽  
Vol 293 (4) ◽  
pp. R1552-R1560 ◽  
Author(s):  
D. A. Martinez ◽  
A. C. Vailas ◽  
R. Vanderby ◽  
R. E. Grindeland
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Wound Healing ◽  
Matrix Metalloproteinase ◽  
Collagen Type ◽  
Male Rats ◽  
Matrix Metalloproteinase 2 ◽  
Type Iii Collagen ◽  
Type I ◽  
Matrix Metalloproteinase 1

Previous data from spaceflight studies indicate that injured muscle and bone heal slowly and abnormally compared with ground controls, strongly suggesting that ligaments or tendons may not repair optimally as well. Thus the objective of this study was to investigate the biochemical and molecular gene expression of the collagen extracellular matrix in response to medial collateral ligament (MCL) injury repair in hindlimb unloaded (HLU) rodents. Male rats were assigned to 3- and 7-wk treatment groups with three subgroups each: sham control, ambulatory healing (Amb-healing), and HLU-healing groups. Amb- and HLU-healing animals underwent bilateral surgical transection of their MCLs, whereas control animals were subjected to sham surgeries. All surgeries were performed under isoflurane anesthesia. After 3 wk or 7 wk of HLU, rats were euthanized and MCLs were surgically isolated and prepared for molecular or biochemical analyses. Hydroxyproline concentration and hydroxylysylpyridinoline collagen cross-link contents were measured by HPLC and showed a substantial decrement in surgical groups. MCL tissue cellularity, quantified by DNA content, remained significantly elevated in all HLU-healing groups vs. Amb-healing groups. MCL gene expression of collagen type I, collagen type III, collagen type V, fibronectin, decorin, biglycan, lysyl oxidase, matrix metalloproteinase-2, and tissue inhibitor of matrix metalloproteinase-1, measured by real-time quantitative PCR, demonstrated differential expression in the HLU-healing groups compared with Amb-healing groups at both the 3- and 7-wk time points. Together, these data suggest that HLU affects dense fibrous connective tissue wound healing and confirms previous morphological and biomechanical data that HLU inhibits the ligament repair processes.

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