scholarly journals Isolation of Type I and Type II Pericytes from Mouse Skeletal Muscles

Author(s):  
Abhijit Nirwane ◽  
Jyoti Gautam ◽  
Yao Yao
Keyword(s):  
Type I ◽  
1980 ◽  
Vol 17 (3) ◽  
pp. 305-315 ◽  
Author(s):  
R. Bradley ◽  
W.V.S. Wueratne

A 5-year-old Friesian stud bull developed a progressive locomotor disorder on return to stud after a period of rest. He had defects in conformation exacerbated by poor condition. The hind limbs were excessively straight. When he stood or moved, the Achilles tendons and their associated muscles were rigid. The disorder clinically resembled spastic paresis of calves. Necropsy showed a degenerative arthropathy in all hind limb joints below the hip. Lesions were also in tendons and skeletal muscles. The M. flexor digitorum superficialis had severe type II cell atrophy with many ring. lobulated and moth-eaten type I cells.


1991 ◽  
Vol 81 (2) ◽  
pp. 267-270 ◽  
Author(s):  
R. G. Cooper ◽  
C. M. Taylor ◽  
J. J. Choo ◽  
J. B. Weiss

1. Capillary density is greater in skeletal muscles comprised of predominantly oxidative (type I) fibres than in those comprised of mainly glycolytic (type II) fibres. In order to investigate further the angiogenic mechanisms involved in muscle capillarization, endothelial-cellstimulating angiogenic factor activities in various rodent skeletal muscles were compared. 2. Eleven untrained adult male Wistar rats were killed and the predominantly oxidative (type I) muscles, soleus and heart, the predominantly glycolytic (type II) muscle, extensor digitorum longus, and the mixed-fibre muscle, gastrocnemius, were removed. Each sample was separately homogenized and centrifuged and the supernatants were diafiltered to isolate the low-molecular-mass fraction containing endothelial-cell-stimulating angiogenic activity. This was assayed for its ability to activate latent collagenase and was expressed as units, where 1 unit represents the percentage activation of the enzyme h−1 (mg of protein in the supernatant)−1. 3. The results (medians and ranges) demonstrated significantly greater endothelial-cell-stimulating angiogenic factor activity in extensor digitorum longus muscle (2.14 units, 0.62–2.87 units, n = 13) than in soleus (0.82 units, 0.59–1.79 units, n = 15), gastrocnemius (0.34 units, 0.28–0.40 units, n = 4) or heart (0.43 units, 0.16–0.52 units, n = 11) (P< 0.01 for each) muscle. 4. These findings suggest that endothelial-cell-stimulating angiogenic activity in muscle is either inversely or not related to the local capillary density, which may be at or near a maximum in physiologically contracting, predominantly oxidative muscles.


2020 ◽  
Author(s):  
Takahiro Asano ◽  
Masaya Tsujii ◽  
Takahiro Iino ◽  
Kazuya Odake ◽  
Akihiro Sudo

Abstract Background: Obesity is a factor for insufficient improvement of motor function for peripheral nerve disorders. The aims of this study were to evaluate the skeletal muscles during denervation and re-innervation following nerve crush injury in ob/ob mice. Methods: Experiments were performed on the skeletal muscles of the hindlimbs in 20 male leptin-deficient (ob/ob) mice and control mice. Firstly, the characteristics of the gastrocnemius muscles in the mice were evaluated by histological analysis, immunohistological analysis, and Sircol-collagen assay after measurement of body weight and wet weight of the skeletal muscles and by walking tracking analysis. In the histological analysis, nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) staining, oil red O staining, and Picro-sirius red staining were performed to assess the type of myofibers, lipid accumulation, and collagen deposition, respectively. Then, the models for denervation and re-innervation were made by crushing the sciatic nerves with smooth forceps. The same assessments were performed on the skeletal muscles of nerve crush models.Results: The wet weight of the gastrocnemius muscles was significantly less in the ob/ob mice than the control mice, whereas body weight was significantly more. Histological analyses demonstrated a smaller cross-sectional area of type II fibers and increase of type I fiber grouping of the skeletal muscles in the ob/ob mice. In addition, there was excessive deposition of lipids and collagens between the myofibers. Following the nerve injury, the recovery of motor function was equal between both groups, while the cross-sectional area of type II fibers was significantly smaller in the ob/ob mice than the control mice at 4 weeks. Furthermore, the denervated muscles showed an increase in collagen deposition to the area of intermyofibers, which were predominant in the ob/ob mice after the nerve injury.Conclusions: The present study showed an increase of collagen deposition, delayed recovery of type II myofibers, and type I fiber grouping during denervation and re-innervation in the skeletal muscles of ob/ob mice. We suggest through these findings that the reduction of contractile force could be one of causes of insufficient improvement in peripheral nerve disorders of obese individuals.


1990 ◽  
Vol 79 (s23) ◽  
pp. 12P-12P
Author(s):  
T. Siddiq ◽  
V. R. Preedy ◽  
J. S. Marway ◽  
P. Richardson ◽  
T. J. Peters

2007 ◽  
Vol 97 (2) ◽  
pp. 1040-1051 ◽  
Author(s):  
R. Luke W. Harris ◽  
Charles T. Putman ◽  
Michelle Rank ◽  
Leo Sanelli ◽  
David J. Bennett

Without intervention after spinal cord injury (SCI), paralyzed skeletal muscles undergo myofiber atrophy and slow-to-fast myofiber type transformations. We hypothesized that chronic spasticity-associated neuromuscular activity after SCI would promote recovery from such deleterious changes. We examined segmental tail muscles of chronic spinal rats with long-standing tail spasticity (7 mo after sacral spinal cord transection; older chronic spinals), chronic spinal rats that experienced less spasticity early after injury (young chronic spinals), and rats without spasticity after transection and bilateral deafferentation (spinal isolated). These were compared with tail muscles of age-matched normal rats. Using immunohistochemistry, we observed myofiber distributions of 15.9 ± 3.5% type I, 18.7 ± 10.7% type IIA, 60.8 ± 12.6% type IID(X), and 2.3 ± 1.3% type IIB (means ± SD) in young normals, which were not different in older normals. Young chronic spinals demonstrated transformations toward faster myofiber types with decreased type I and increased type IID(X) paralleled by atrophy of all myofiber types compared with young normals. Spinal isolated rats also demonstrated decreased type I myofiber proportions and increased type II myofiber proportions, and severe myofiber atrophy. After 4 mo of complete spasticity (older chronic spinals), myofiber type transformations were reversed, with no significant differences in type I, IIA, IID(X), or IIB proportions compared with age-matched normals. Moreover, after this prolonged spasticity, type I, IIA, and IIB myofibers recovered from atrophy, and type IID(X) myofibers partially recovered. Our results indicate that early after transection or after long-term spinal isolation, relatively inactive tail myofibers atrophy and transform toward faster myofiber types. However, long-term spasticity apparently produces neuromuscular activity that promotes recovery of myofiber types and myofiber sizes.


Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.


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