scholarly journals Passive Skeletal Muscle Excursion after Tendon Rupture Correlates with Increased Collagen Content in Muscle

2014 ◽  
Vol 55 (5) ◽  
pp. 1395 ◽  
Author(s):  
Il Hyun Koh ◽  
Ho Jung Kang ◽  
Sang Woo Jeon ◽  
Jae Han Park ◽  
Yun Rak Choi
Keyword(s):  
Skeletal Muscle ◽  
Tendon Rupture ◽  
Collagen Content ◽  
Muscle Excursion

Increased collagen content in insulin-resistant skeletal muscle

2006 ◽  
Vol 290 (3) ◽  
pp. E560-E565 ◽  
Author(s):  
Rachele Berria ◽  
Lishan Wang ◽  
Dawn K. Richardson ◽  
Jean Finlayson ◽  
Renata Belfort ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Collagen Content ◽  
Matrix Composition ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Insulin Resistant ◽  
Obese Subjects ◽  
Type 2 Diabetic

Oversupply and underutilization of lipid fuels are widely recognized to be strongly associated with insulin resistance in skeletal muscle. Recent attention has focused on the mechanisms underlying this effect, and defects in mitochondrial function have emerged as a potential player in this scheme. Because evidence indicates that lipid oversupply can produce abnormalities in extracellular matrix composition and matrix changes can affect the function of mitochondria, the present study was undertaken to determine whether muscle from insulin-resistant, nondiabetic obese subjects and patients with type 2 diabetes mellitus had increased collagen content. Compared with lean control subjects, obese and type 2 diabetic subjects had reduced muscle glucose uptake ( P < 0.01) and decreased insulin stimulation of tyrosine phosphorylation of insulin receptor substrate-1 and its ability to associate with phosphatidylinositol 3-kinase ( P < 0.01 and P < 0.05). Because it was assayed by total hydroxyproline content, collagen abundance was increased in muscle from not only type 2 diabetic patients but also nondiabetic obese subjects (0.26 ± 0.05, 0.57 ± 0.18, and 0.67 ± 0.20 μg/mg muscle wet wt, lean controls, obese nondiabetics, and type 2 diabetics, respectively), indicating that hyperglycemia itself could not be responsible for this effect. Immunofluorescence staining of muscle biopsies indicated that there was increased abundance of types I and III collagen. We conclude that changes in the composition of the extracellular matrix are a general characteristic of insulin-resistant muscle.

scholarly journals Skeletal Muscle Fibrosis in Pancreatic Cancer Patients with Respect to Survival

2018 ◽  
Vol 2 (3) ◽  
Author(s):  
Sarah M Judge ◽  
Rachel L Nosacka ◽  
Daniel Delitto ◽  
Michael H Gerber ◽  
Miles E Cameron ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Body Weight ◽  
Cellular Response ◽  
Cancer Cachexia ◽  
Cancer Control ◽  
Body Weight Loss ◽  
Collagen Content ◽  
Calcium Deposition ◽  
Control Subjects

Abstract Background Cancer cachexia is a catabolic condition characterized by skeletal muscle wasting, consequent to tumor burden, which negatively impacts tolerance to cancer therapies and contributes to increased mortality. Partly because of the limited knowledge of the underlying mechanisms of cancer cachexia derived from human studies, however, the ability to therapeutically intervene remains elusive. The purpose of the current study was therefore to better define the phenotype of skeletal muscle obtained from patients with pancreatic ductal adenocarcinoma (PDAC), which has one of the highest rates of cachexia. Methods Morphological analyses were performed on rectus abdominis muscle biopsies obtained from resectable PDAC patients undergoing tumor resection surgery (N = 20) and from weight-stable non-cancer control subjects undergoing benign abdominal surgery (N = 16). PDAC patients with a body weight loss of greater than 5% during the previous 6 months were considered cachectic (N = 15). Statistical tests were two sided. Results Skeletal muscle from cachectic PDAC patients had increased collagen content compared with non-cancer control subjects (1.43% vs 9.66%, P = .0004, Dunn test). Across all PDAC patients, collagen content positively correlated with body weight loss (P = .0016, r = 0.672), was increased in patients with lymph node metastasis (P = .007, Mann-Whitney U test), and was associated with survival on univariate (HR = 1.08, 95% confidence interval [CI] = 1.02 to 1.04, P = .008) and multivariable analyses (HR = 1.08, 95% CI = 1.00 to 1.17, P = .038). Cachectic PDAC patients also displayed increased lipid deposition (2.63% vs 5.72%, P = .042), infiltration of CD68+ macrophages (63.6 cells/mm2 vs 233.8 cells/mm2, P = .0238), calcium deposition (0.21% vs 2.51%, P = .030), and evidence of deficient cellular quality control mechanisms (Mann-Whitney U test). Transcriptional profiling of all patients supported these findings by identifying gene clusters related to wounding, inflammation, and cellular response to TGF-β upregulated in cachectic PDAC patients compared with non-cancer control subjects. Conclusions To our knowledge, this work is the first to demonstrate increased collagen content in cachectic PDAC patients that is associated with poor survival.

Temporary fatigue and altered extracellular matrix in skeletal muscle during progression of heart failure in rats

2009 ◽  
Vol 297 (1) ◽  
pp. R26-R33 ◽  
Author(s):  
Tommy A. Rehn ◽  
Bengt Å. Borge ◽  
Per K. Lunde ◽  
Morten Munkvik ◽  
Marianne Lunde Sneve ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Muscle Fatigue ◽  
Hind Limb ◽  
Collagen Content ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Skeletal Muscle Fatigue

Patients with congestive heart failure (CHF) experience increased skeletal muscle fatigue. The mechanism underlying this phenomenon is unknown, but a deranged extracellular matrix (ECM) might be a contributing factor. Hence, we examined ECM components and regulators in a rat postinfarction model of CHF. At various time points during a 3.5 mo-period after induction of CHF in rats by left coronary artery ligation, blood, interstitial fluid (IF), and muscles were sampled. Isoflurane anesthesia was employed during all surgical procedures. IF was extracted by wicks inserted intermuscularly in a hind limb. We measured cytokines in plasma and IF, whereas matrix metalloproteinase (MMP) activity and collagen content, as well as the level of glycosaminoglycans and hyaluronan were determined in hind limb muscle. In vivo fatigue protocols of the soleus muscle were performed at 42 and 112 days after induction of heart failure. We found that the MMP activity and collagen content in the skeletal muscles increased significantly at 42 days after induction of CHF, and these changes were time related to increased skeletal muscle fatigability. These parameters returned to sham levels at 112 days. VEGF in IF was significantly lower in CHF compared with sham-operated rats at 3 and 10 days, but no difference was observed at 112 days. We conclude that temporary alterations in the ECM, possibly triggered by VEGF, are related to a transient development of skeletal muscle fatigue in CHF.

scholarly journals Functional Deficits are Explained by Plantarflexor Remodeling Following Achilles Tendon Rupture Repair: Preliminary Findings

2018 ◽  
Author(s):  
Josh R. Baxter ◽  
Todd J. Hullfish ◽  
Wen Chao
Keyword(s):  
Skeletal Muscle ◽  
Achilles Tendon ◽  
Tendon Rupture ◽  
Achilles Tendon Rupture ◽  
Medial Gastrocnemius ◽  
Fascicle Length ◽  
Functional Deficits ◽  
Limited Function ◽  
Poor Outcomes ◽  
Muscle Remodeling

AbstractAchilles tendon ruptures are painful injuries that often lead to long-term functional deficits. Despite the prevalence of these injuries, the mechanism responsible for limited function has not yet been established. Therefore, the purpose of this study was to present preliminary findings that support a hypothesis that skeletal muscle remodeling is the driving factor of poor outcomes in some patients. Biomechanical and ultrasonography assessments were performed on a patient that presented with poor functional outcomes 2.5 years after a surgically-repaired acute Achilles tendon rupture. Single-leg heel raise function was decreased by 70% in the affected limb while walking mechanics showed no deficits. Ultrasonography revealed that the affected limb had shorter, more pennated, and less thick medial gastrocnemius muscles compared to the unaffected limb. A simple computational model of a maximal-effort plantarflexion contraction was employed to test the implications of muscle remodeling on single-leg heel raise function. Subject-specific fascicle length and pennation measurements explained deficits in ankle work and power that strongly agreed with experimentally measured values using motion capture. These preliminary findings support the hypothesis that skeletal muscle goes extensively remodels in response to a ruptured tendon, which reduces the amount of work and power the joint can generate. This multidisciplinary framework of biomechanical, imaging, and computational modeling provides a unique platform for studying the complex interactions between structure and function in patients recovering from Achilles tendon injuries.

scholarly journals Collagen content does not alter the passive mechanical properties of fibrotic skeletal muscle inmdxmice

2014 ◽  
Vol 306 (10) ◽  
pp. C889-C898 ◽  
Author(s):  
Lucas R. Smith ◽  
Elisabeth R. Barton
Keyword(s):  
Mechanical Properties ◽  
Skeletal Muscle ◽  
Packing Density ◽  
Dynamic Stiffness ◽  
Relative Viscosity ◽  
Collagen Content ◽  
Mdx Mice ◽  
Passive Stiffness ◽  
Muscle Fibrosis ◽  
Collagen Organization

Many skeletal muscle diseases are associated with progressive fibrosis leading to impaired muscle function. Collagen within the extracellular matrix is the primary structural protein providing a mechanical scaffold for cells within tissues. During fibrosis collagen not only increases in amount but also undergoes posttranslational changes that alter its organization that is thought to contribute to tissue stiffness. Little, however, is known about collagen organization in fibrotic muscle and its consequences for function. To investigate the relationship between collagen content and organization with muscle mechanical properties, we studied mdx mice, a model for Duchenne muscular dystrophy (DMD) that undergoes skeletal muscle fibrosis, and age-matched control mice. We determined collagen content both histologically, with picosirius red staining, and biochemically, with hydroxyproline quantification. Collagen content increased in the mdx soleus and diaphragm muscles, which was exacerbated by age in the diaphragm. Collagen packing density, a parameter of collagen organization, was determined using circularly polarized light microscopy of picosirius red-stained sections. Extensor digitorum longus (EDL) and soleus muscle had proportionally less dense collagen in mdx muscle, while the diaphragm did not change packing density. The mdx muscles had compromised strength as expected, yet only the EDL had a significantly increased elastic stiffness. The EDL and diaphragm had increased dynamic stiffness and a change in relative viscosity. Unexpectedly, passive stiffness did not correlate with collagen content and only weakly correlated with collagen organization. We conclude that muscle fibrosis does not lead to increased passive stiffness and that collagen content is not predictive of muscle stiffness.

scholarly journals Skeletal muscle fibrosis is associated with decreased muscle inflammation and weakness in patients with chronic kidney disease

2018 ◽  
Vol 315 (6) ◽  
pp. F1658-F1669 ◽  
Author(s):  
Matthew K. Abramowitz ◽  
William Paredes ◽  
Kehao Zhang ◽  
Camille R. Brightwell ◽  
Julia N. Newsom ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Collagen I ◽  
Collagen Content ◽  
Muscle Pathology ◽  
Leg Extension ◽  
Muscle Fibrosis ◽  
Tnf Α ◽  
Skeletal Muscle Fibrosis

Muscle dysfunction is an important cause of morbidity among patients with chronic kidney disease (CKD). Although muscle fibrosis is present in a CKD rodent model, its existence in humans and its impact on physical function are currently unknown. We examined isometric leg extension strength and measures of skeletal muscle fibrosis and inflammation in vastus lateralis muscle from CKD patients ( n = 10) and healthy, sedentary controls ( n = 10). Histochemistry and immunohistochemistry were used to assess muscle collagen and macrophage and fibro/adipogenic progenitor (FAP) cell populations, and RT-qPCR was used to assess muscle-specific inflammatory marker expression. Muscle collagen content was significantly greater in CKD compared with control (18.8 ± 2.1 vs. 11.7 ± 0.7% collagen area, P = 0.008), as was staining for collagen I, pro-collagen I, and a novel collagen-hybridizing peptide that binds remodeling collagen. Muscle collagen was inversely associated with leg extension strength in CKD ( r = −0.74, P = 0.01). FAP abundance was increased in CKD, was highly correlated with muscle collagen ( r = 0.84, P < 0.001), and was inversely associated with TNF-α expression ( r = −0.65, P = 0.003). TNF-α, CD68, CCL2, and CCL5 mRNA were significantly lower in CKD than control, despite higher serum TNF-α and IL-6. Immunohistochemistry confirmed fewer CD68+ and CD11b+ macrophages in CKD muscle. In conclusion, skeletal muscle collagen content is increased in humans with CKD and is associated with functional parameters. Muscle fibrosis correlated with increased FAP abundance, which may be due to insufficient macrophage-mediated TNF-α secretion. These data provide a foundation for future research elucidating the mechanisms responsible for this newly identified human muscle pathology.

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