degradative enzymes
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2021 ◽  
Author(s):  
Xuancheng Zhang ◽  
Ang Li ◽  
Kang Han ◽  
He Zhang ◽  
Xiaoqiao Huangfu ◽  
...  

Abstract Background: Glucocorticoids (GCs) injections are commonly used to relieve pain and improve function in patients with multiple shoulder disability, they cause detrimental effects on the rotator cuff tendons. Adipose stem cell-derived exosomes (ASC-Exos) reportedly recover impaired tendon matrix metabolism by maintaining tissue homeostasis. It is unclear whether additional ASC-Exos treatment overrides the detrimental effects of GCs without interfering with their anti-inflammatory effects.Methods: The in vitro studies included inflammatory analysis and cytoprotective analysis. In the inflammatory analysis, rat raw cells were treated with saline, GCs, or GCs + ASC-Exos and evaluated regarding cellular proliferation, migration, and secretion of inflammatory-related cytokines. In the cytoprotective analysis, rat tenocytes were treated with saline, GCs, or GCs + ASC-Exos and evaluated regarding cellular proliferation, migration, senescence, apoptosis, and transcription of tenocytic genes. In the in vivo studies, a subacromial injection of saline, GCs, or GCs + ASC-Exos was performed in a chronic injured-intact rotator cuff rat model. Histological and biomechanical analysis were performed 1 week to evaluate the protective effect of ASC-Exos against GCs-induced detriments on injured-intact in rotator cuffs.Results: In the in vitro inflammatory analysis, GCs treatment significantly decreased the proliferation, migration, and secretion of pro-inflammatory cytokines in raw cells, and increased the secretion of anti-inflammatory cytokines; additional ASC-Exos treatment further significantly decreased the secretion of pro-inflammatory cytokines and increased the secretion of anti-inflammatory cytokines, while restoring GCs-suppressed cellular proliferation and migration. In the in vitro cytoprotective analysis, GCs treatment significantly decreased the proliferation, migration, and transcription of tenocytic matrix molecules of tenocytes, and significantly increased their senescence, apoptosis, and transcription of ROS and tenocytic degradative enzymes; additional ASC-Exos treatment significantly improved the GCs-suppressed cellular proliferation, migration, and transcription of tenocytic matrix molecules, transcription of tenocytic degradative enzyme inhibitors, and significantly decreased the GCs-induced cell senescence, apoptosis, and transcription of ROS and tenocytic degradative enzymes. In the in vivo studies, an additional ASC-Exos injection restored the impaired histological and biomechanical properties owing to GCs administration.Conclusion: ASC-Exos may exert a stronger anti-inflammatory effect in combination with GCs, and override their detrimental effects on the rotator cuff.


2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Gessesse Kebede ◽  
Tekle Tafese ◽  
Ebrahim M. Abda ◽  
M. Kamaraj ◽  
Fassil Assefa

The discharge of hydrocarbons and their derivatives to environments due to human and/or natural activities cause environmental pollution (soil, water, and air) and affect the natural functioning of an ecosystem. To minimize or eradicate environmental pollution by hydrocarbon contaminants, studies showed strategies including physical, chemical, and biological approaches. Among those strategies, the use of biological techniques (especially bacterial biodegradation) is critically important to remove hydrocarbon contaminants. The current review discusses the insights of major factors that enhance or hinder the bacterial bioremediation of hydrocarbon contaminants (aliphatic, aromatic, and polyaromatic hydrocarbons) in the soil. The key factors limiting the overall hydrocarbon biodegradation are generally categorized as biotic factors and abiotic factors. Among various environmental factors, temperature range from 30 to 40°C, pH range from 5 to 8, moisture availability range from 30 to 90%, carbon/nitrogen/phosphorous (C/N/P; 100:20:1) ratio, and 10–40% of oxygen for aerobic degradation are the key factors that show positive correlation for greatest hydrocarbon biodegradation rate by altering the activities of the microbial and degradative enzymes in soil. In addition, the formation of biofilm and production of biosurfactants in hydrocarbon-polluted soil environments increase microbial adaptation to low bioavailability of hydrophobic compounds, and genes that encode for hydrocarbon degradative enzymes are critical for the potential of microbes to bioremediate soils contaminated with hydrocarbon pollutants. Therefore, this review works on the identification of factors for effective hydrocarbon biodegradation, understanding, and optimization of those factors that are essential and critical.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1593
Author(s):  
Yunfei Li ◽  
Yulia Liem ◽  
Zaitunnatakhin Zamli ◽  
Niall Sullivan ◽  
Enrico Dall’Ara ◽  
...  

Background: The purpose of this study was to investigate the relationship between the expression of key degradative enzymes by chondrocytes and the microarchitectural and mineral properties of subchondral bone across different stages of cartilage degradation in human hip osteoarthritis (OA). Methods: Osteochondral samples at different stages of cartilage degradation were collected from 16 femoral heads with OA. Osteochondral samples with normal cartilage were collected from seven femoral heads with osteoporosis. Microcomputed tomography was used for the investigation of subchondral bone microarchitecture and mineral densities. Immunohistochemistry was used to study the expression and distribution of MMP13 and ADAMTS4 in cartilage. Results: The microarchitecture and mineral properties of the subchondral plate and trabecular bone in OA varied with the severity of the degradation of the overlying cartilage. Chondrocytes expressing MMP13 and ADAMTS4 are mainly located in the upper zone(s) of cartilage regardless of the histopathological grades. The zonal expression of these enzymes in OA (i.e., the percentage of positive cells in the superficial, middle, and deep zones), rather than their overall expression (the percentage of positive cells in the full thickness of the cartilage), exhibited significant variation in relation to the severity of cartilage degradation. The associations between the subchondral bone properties and zonal and overall expression of these enzymes in the cartilage were generally weak or nonsignificant. Conclusions: Phenotypic changes in chondrocytes and remodelling of subchondral bone proceed at different rates throughout the process of cartilage degradation. Biological influences are more important for cartilage degradation at early stages, while biomechanical damage to the compromised tissue may outrun the phenotypic change of chondrocytes and is critical in the advanced stages.


2021 ◽  
Vol 9 (11) ◽  
pp. 2269
Author(s):  
Sayed Golam Mohiuddin ◽  
Sreyashi Ghosh ◽  
Han G. Ngo ◽  
Shayne Sensenbach ◽  
Prashant Karki ◽  
...  

Cellular self-digestion is an evolutionarily conserved process occurring in prokaryotic cells that enables survival under stressful conditions by recycling essential energy molecules. Self-digestion, which is triggered by extracellular stress conditions, such as nutrient depletion and overpopulation, induces degradation of intracellular components. This self-inflicted damage renders the bacterium less fit to produce building blocks and resume growth upon exposure to fresh nutrients. However, self-digestion may also provide temporary protection from antibiotics until the self-digestion-mediated damage is repaired. In fact, many persistence mechanisms identified to date may be directly or indirectly related to self-digestion, as these processes are also mediated by many degradative enzymes, including proteases and ribonucleases (RNases). In this review article, we will discuss the potential roles of self-digestion in bacterial persistence.


2021 ◽  
Vol 22 (17) ◽  
pp. 9239
Author(s):  
Jacqueline T. Hecht ◽  
Alka C. Veerisetty ◽  
Mohammad G. Hossain ◽  
Debabrata Patra ◽  
Frankie Chiu ◽  
...  

Pseudoachondroplasia (PSACH), a short limb skeletal dysplasia associated with premature joint degeneration, is caused by misfolding mutations in cartilage oligomeric matrix protein (COMP). Here, we define mutant-COMP-induced stress mechanisms that occur in articular chondrocytes of MT-COMP mice, a murine model of PSACH. The accumulation of mutant-COMP in the ER occurred early in MT-COMP articular chondrocytes and stimulated inflammation (TNFα) at 4 weeks, and articular chondrocyte death increased at 8 weeks while ER stress through CHOP was elevated by 12 weeks. Importantly, blockage of autophagy (pS6), the major mechanism that clears the ER, sustained cellular stress in MT-COMP articular chondrocytes. Degeneration of MT-COMP articular cartilage was similar to that observed in PSACH and was associated with increased MMPs, a family of degradative enzymes. Moreover, chronic cellular stresses stimulated senescence. Senescence-associated secretory phenotype (SASP) may play a role in generating and propagating a pro-degradative environment in the MT-COMP murine joint. The loss of CHOP or resveratrol treatment from birth preserved joint health in MT-COMP mice. Taken together, these results indicate that ER stress/CHOP signaling and autophagy blockage are central to mutant-COMP joint degeneration, and MT-COMP mice joint health can be preserved by decreasing articular chondrocyte stress. Future joint sparing therapeutics for PSACH may include resveratrol.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mark B. Wiley ◽  
Pedro A. Perez ◽  
Donovan A. Argueta ◽  
Bryant Avalos ◽  
Courtney P. Wood ◽  
...  

The endocannabinoid system is expressed in cells throughout the body and controls a variety of physiological and pathophysiological functions. We describe robust and reproducible UPLC-MS/MS-based methods for analyzing metabolism of the endocannabinoids, 2-arachidonoyl-sn-glycerol and arachidonoyl ethanolamide, and related monoacylglycerols (MAGs) and fatty acid ethanolamides (FAEs), respectively, in mouse mucosal tissues (i.e., intestine and lung). These methods are optimized for analysis of activity of the MAG biosynthetic enzyme, diacylglycerol lipase (DGL), and MAG degradative enzymes, monoacylglycerol lipase (MGL) and alpha/beta hydrolase domain containing-6 (ABHD6). Moreover, we describe a novel UPLC-MS/MS-based method for analyzing activity of the FAE degradative enzyme, fatty acid amide hydrolase (FAAH), that does not require use of radioactive substrates. In addition, we describe in vivo pharmacological methods to inhibit MAG biosynthesis selectively in the mouse small-intestinal epithelium. These methods will be useful for profiling endocannabinoid metabolism in rodent mucosal tissues in health and disease.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Allison Mixon ◽  
Andrew Savage ◽  
Ahmed Suparno Bahar-Moni ◽  
Malek Adouni ◽  
Tanvir Faisal

AbstractMatrix metalloproteinases (MMPs) play a crucial role in enzymatically digesting cartilage extracellular matrix (ECM) components, resulting in degraded cartilage with altered mechanical loading capacity. Overexpression of MMPs is often caused by trauma, physiologic conditions and by disease. To understand the synergistic impact MMPs have on cartilage biomechanical properties, MMPs from two subfamilies: collagenase (MMP-1) and gelatinase (MMP-9) were investigated in this study. Three different ratios of MMP-1 (c) and MMP-9 (g), c1:g1, c3:g1 and c1:g3 were considered to develop a degradation model. Thirty samples, harvested from bovine femoral condyles, were treated in groups of 10 with one concentration of enzyme mixture. Each sample was tested in a healthy state prior to introducing degradative enzymes to establish a baseline. Samples were subjected to indentation loading up to 20% bulk strain. Both control and treated samples were mechanically and histologically assessed to determine the impact of degradation. Young’s modulus and peak load of the tissue under indentation were compared between the control and degraded cartilage explants. Cartilage degraded with the c3:g1 enzyme concentration resulted in maximum 33% reduction in stiffness and peak load compared to the other two concentrations. The abundance of collagenase is more responsible for cartilage degradation and reduced mechanical integrity.


2021 ◽  
Author(s):  
Jacqueline T Hecht ◽  
Alka C Veerisetty ◽  
Mohammad G Hossain ◽  
Debabrata Patra ◽  
Frankie Chiu ◽  
...  

Pseudoachondroplasia (PSACH), a short limb skeletal dysplasia, associated with premature joint degeneration is caused by misfolding mutations in cartilage oligomeric matrix protein (COMP). Here, we define mutant-COMP-induced stress mechanisms that occur in articular chondrocytes of MT-COMP mice, a murine model of PSACH. The accumulation of mutant-COMP in the ER occurred early in MT-COMP articular chondrocytes and stimulated inflammation (TNFα) at 4 wks. Articular chondrocyte death increased at 8 wks and ER stress through CHOP was elevated by 12 wks. Importantly, blockage of autophagy (pS6), the major mechanism which clears the ER, sustained cellular stress in MT-COMP articular chondrocytes. Degeneration of MT-COMP articular cartilage was similar to that observed in PSACH and was associated with increased MMPs, degradative enzymes. Moreover, chronic cellular stresses stimulated senescence. Senescence-associated secretory phenotype (SASP) may play a role in generating and propagating a pro-degradative environment in the MT-COMP murine joint. The loss of CHOP or resveratrol treatment from birth preserved joint health in MT-COMP mice. Taken together, these results indicate that ER stress/CHOP signaling and autophagy blockage are central to mutant-COMP joint degeneration and MT-COMP mice joint health can be preserved by decreasing articular chondrocyte stress. Future joint sparing therapeutics for PSACH may include resveratrol.


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