Proteolytic 'defences' and the accumulation of oxidized polypeptides in cataractogenesis and atherogenesis

2003 ◽  
Vol 70 ◽  
pp. 135-146 ◽  
Author(s):  
Roger T. Dean ◽  
Rachael Dunlop ◽  
Peter Hume ◽  
Ken J. Rodgers
Keyword(s):  
Protein Oxidation ◽  
Oxidative Burst ◽  
Connective Tissues ◽  
Oxidized Proteins ◽  
Accelerated Degradation ◽  
Experimental Systems ◽  
Age Related ◽  
Low Levels ◽  
And Control ◽  
Neutrophil Oxidative Burst

Over the last few years, it has been clearly established that normal plasma contains low levels of oxidized polypeptides, and that these accumulate in tissues during several age-related pathologies. In contrast, normal mammalian aging, contrary to conventional dogma, is not clearly associated with enhanced levels of oxidized proteins, except in extracellular connective tissues, whose proteins can, for example, be oxidized by the neutrophil oxidative burst. Since mildly oxidized proteins are susceptible to accelerated degradation in most experimental systems, the question arises as to how the accumulation of oxidized proteins can take place. Such accumulation requires an excess of production (or deposition) over removal, which might reflect alterations in capacity or rate of production or removal. This chapter discusses our presently limited knowledge of rates and control of proteolysis of oxidized proteins in two pathologies, cataractogenesis and atherogenesis. It commences with a brief summary of current understanding of the mechanisms of protein oxidation, and of the observed accumulation of oxidized proteins in several pathologies.

scholarly journals Plasma Protein Oxidation and Its Correlation with Antioxidant Potential During Human Aging

2010 ◽  
Vol 29 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Kanti Bhooshan Pandey ◽  
Mohd Murtaza Mehdi ◽  
Pawan Kumar Maurya ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Plasma Protein ◽  
Protein Oxidation ◽  
Cellular Systems ◽  
Antioxidant Potential ◽  
Protein Carbonyls ◽  
Oxidized Proteins ◽  
Oxidative Damages ◽  
Age Related ◽  
Age Dependent

Previous studies have indicated that the main molecular characteristic of aging is the progressive accumulation of oxidative damages in cellular macromolecules. Proteins are one of the main molecular targets of age-related oxidative stress, which have been observed during aging process in cellular systems. Reactive oxygen species (ROS) can lead to oxidation of amino acid side chains, formation of protein-protein cross-linkages, and oxidation of the peptide backbones. In the present study, we report the age-dependent oxidative alterations in biomarkers of plasma protein oxidation: protein carbonyls (PCO), advanced oxidation protein products (AOPPs) and plasma total thiol groups (T-SH) in the Indian population and also correlate these parameters with total plasma antioxidant potential. We show an age dependent decrease in T-SH levels and increase in PCO and AOPPs level. The alterations in the levels of these parameters correlated significantly with the total antioxidant capacity of the plasma. The levels of oxidized proteins in plasma provide an excellent biomarker of oxidative stress due to the relative long half-life of such oxidized proteins.

scholarly journals Apoptosis in the Extraosseous Calcification Process

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 131
Author(s):  
Federica Boraldi ◽  
Francesco Demetrio Lofaro ◽  
Daniela Quaglino
Keyword(s):  
Genetic Basis ◽  
Membrane Vesicles ◽  
Matrix Vesicles ◽  
Apoptotic Bodies ◽  
Connective Tissues ◽  
Mineralization Process ◽  
Mitochondrial Alterations ◽  
Age Related ◽  
And Oxidative Stress ◽  
And Cartilage

Extraosseous calcification is a pathologic mineralization process occurring in soft connective tissues (e.g., skin, vessels, tendons, and cartilage). It can take place on a genetic basis or as a consequence of acquired chronic diseases. In this last case, the etiology is multifactorial, including both extra- and intracellular mechanisms, such as the formation of membrane vesicles (e.g., matrix vesicles and apoptotic bodies), mitochondrial alterations, and oxidative stress. This review is an overview of extraosseous calcification mechanisms focusing on the relationships between apoptosis and mineralization in cartilage and vascular tissues, as these are the two tissues mostly affected by a number of age-related diseases having a progressively increased impact in Western Countries.

scholarly journals Autobiographical Memory in Normal Ageing and Dementia

1991 ◽  
Vol 4 (4) ◽  
pp. 235-248 ◽  
Author(s):  
Harvey J. Sagar ◽  
Edith V. Sullivan ◽  
Suzanne Corkin
Keyword(s):  
Memory Function ◽  
Early Adulthood ◽  
Normal Subjects ◽  
Elderly Subjects ◽  
Retrieval Cues ◽  
Age Related ◽  
Normal Ageing ◽  
Severity Of Dementia ◽  
And Control ◽  
Cue Words

Autobiographical memories in young and elderly normal subjects are drawn mostly from the recent past but elderly subjects relate a second peak of memories from early adulthood. Memory for remote past public events is relatively preserved in dementia, possibly reflecting integrity of semantic relative to episodic memory. We examined recall of specific, consistent autobiographical episodes in Alzheimer's disease (AD) in response to cue words. Patients and control subjects drew most memories from the recent 20 years: episode age related to anterograde memory function but not subject age or dementia. Subjects also related a secondary peak of memories from early adulthood; episode age related to subject age and severity of dementia. The results suggest that preferential recall of memories from early adulthood is based on the salience of retrieval cues, altered by age and dementia, superimposed on a temporal gradient of semantic memory. Further, AD shows behavioural similarity to normal ageing.

scholarly journals TGIF1 Gene Silencing in Tendon-Derived Stem Cells Improves the Tendon-to-Bone Insertion Site Regeneration

2015 ◽  
Vol 37 (6) ◽  
pp. 2101-2114 ◽  
Author(s):  
Liyang Chen ◽  
Chaoyin Jiang ◽  
Shashi Ranjan Tiwari ◽  
Amrit Shrestha ◽  
Pengcheng Xu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Gene Silencing ◽  
Healing Process ◽  
Insertion Site ◽  
Tendon Repair ◽  
Scar Tissue ◽  
Connective Tissues ◽  
Expression Rate ◽  
Low Levels ◽  
Derivatives Of

Background/Aims: The slow healing process of tendon-to-bone junctions can be accelerated via implanted tendon-derived stem cells (TDSCs) with silenced transforming growth interacting factor 1 (TGIF1) gene. Tendon-to-bone insertion site is the special form of connective tissues derivatives of common connective progenitors, where TGF-β plays bidirectional effects (chondrogenic or fibrogenic) through different signaling pathways at different stages. A recent study revealed that TGF-β directly induces the chondrogenic gene Sox9. However, TGIF1 represses the expression of the cartilage master Sox9 gene and changes its expression rate against the fibrogenesis gene Scleraxis (Scx). Methods: TGIF1 siRNA was transduced or TGIF1 was over-expressed in tendon-derived stem cells. Following suprapinatus tendon repair, rats were either treated with transduced TDSCs or nontransduced TDSCs. Histologic examination and Western blot were performed in both groups. Results: In this study, the silencing of TGIF1 significantly upregulated the chondrogenic genes and markers. Similarly, TGIF1 inhibited TDSC differentiation into cartilage via interactions with TGF-β-activated Smad2 and suppressed the phosphorylation of Smad2. The area of fibrocartilage at the tendon-bone interface was significantly increased in the TGIF1 (-) group compared with the control and TGIF1-overexpressing groups in the early stages of the animal model. The interface between the tendon and bone showed a increase of new bone and fibrocartilage in the TGIF1 (-) group at 4 weeks. Fibrovascular scar tissue was observed in the TGIF1-overexpressing group and the fibrin glue only group. Low levels of fibrocartilage and fibrovascular scar tissue were found in the TDSCs group. Conclusion: Collectively, this study shows that the tendon-derived stem cell modified with TGIF1 gene silencing has promising effects on tendon-to-bone healing which can be further explored as a therapeutic tool in regenerative medicine.

Biology and Control of Black Nightshade (Solanum nigrum) in Cotton (Gossypium hirsutum)

1991 ◽  
Vol 5 (4) ◽  
pp. 713-722 ◽  
Author(s):  
Paul E. Keeley ◽  
Robert J. Thullen
Keyword(s):  
Soil Moisture ◽  
Sprinkler Irrigation ◽  
Yield Losses ◽  
Accelerated Degradation ◽  
Black Nightshade ◽  
Excellent Control ◽  
Late Application ◽  
And Control ◽  
Field Plots ◽  
Weed Resistance

A 4-yr study (1985, 1987, 1988, 1989) was conducted on the same field plots at Shafter, CA to evaluate the efficacy of prometryn in controlling black nightshade on planting beds of cotton. Two rates (1.7 and 2.2 kg ai ha–1) were applied at two times (mid March before the preplant irrigation and early April at cotton planting) each year. Incorporation of prometryn into moist planting beds with a powered rotary tiller operated at 10 cm deeper resulted in excellent control of black nightshade under low to moderate weed pressure in 1985 and 1987. Control of nightshade with early and late applications of 1.7 kg ha–1of prometryn under high weed pressure in 1988 was only 70% at harvest, and yield losses of cotton averaged 25%. Yields of cotton treated with 2.2 kg ha–1of prometryn in 1988 were not significantly different from weed-free plots. Only the late application of 2.2 kg ha–1of prometryn prevented significant cotton losses under extreme weed pressure in 1989. Cotton yield losses with the other prometryn treatments ranged from 78 to 100%. Losses of cotton in weedy-check plots that received only cultivation ranged from 22% in the absence of rain or irrigation at cotton planting in 1987 to as much as 100% when rain fell in 1988 or plots were irrigated at planting in 1989. Plots hoed one time 4 wk after cotton planting yielded an average of 84% as much seed cotton as weed-free plots. In an attempt to determine why the efficacy of prometryn declined between 1985 and 1989, several experiments were conducted in 1988 to 1990 to discover reasons for this poor control of nightshade. Because efforts failed to provide evidence for the movement of the herbicide with water, the development of weed resistance to prometryn, or accelerated degradation of this herbicide in soil, increasing weed seed populations in soil were believed to have contributed greatly to the declining nightshade control from prometryn. The fact that prometryn applied and incorporated into flat soil provided excellent control of nightshade in 1990 under sprinkler irrigation indicated that both soil moisture and incorporation techniques limited activity of prometryn in planting beds in 1988 and 1989. Incomplete control of nightshade plus good soil moisture at planting contributed to the high weed populations in 1988 and 1989.

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