scholarly journals WOUND HEALING AND COLLAGEN FORMATION

1964 ◽  
Vol 22 (2) ◽  
pp. 365-398 ◽  
Author(s):  
Russell Ross ◽  
Earl P. Benditt
Keyword(s):  
Endoplasmic Reticulum ◽  
Ascorbic Acid ◽  
Messenger Rna ◽  
Complete Disappearance ◽  
Extracellular Material ◽  
Material Characteristic ◽  
Collagen Formation ◽  
Hydroxyamino Acids ◽  
Curved Paths ◽  
Filamentous Material

The changes in scorbutic wounds following the administration of ascorbic acid have been investigated using the techniques of electron microscopy, histochemistry, and autoradioggraphy. Particular attention has been paid to the changes seen in the endoplasmic reticulum of the fibroblasts and to the identity of the extracellular filamentous material characteristic of scorbutic wounds. Seven-day-old wounds in scorbutic guinea pigs were examined prior to and from one to 72 hours following the administration of vitamin C. Fibroblasts from wounds of normal animals demonstrate a characteristic configuration of the ribosomes of the endoplasmic reticulum which is suggested to be analogous to polyribosomes described in cells synthesizing protein such as the reticulocyte. Tangential views of the membranes of the ergastoplasm show the ribosomes to be grouped in paired rows which take both straight and curved paths. This configuration is lost in scurvy and can be seen to begin to reappear as early as 4 hours after giving ascorbic acid. With increasing time, the morphology of the ribosomal aggregates approximates that seen in normal cells, so that by 24 hours their reorientation is complete. It is suggested that one of the disturbances in scurvy may relate to an alteration either in messenger RNA, in the ability of the ribosomes to relate to the messenger, or in the membranes of the ergastoplasm. In addition, the lack of formation of hydroxyamino acids necessary for completing collagen synthesis may be related to the architecture of the ribosomal aggregates. Extracellular collagen fibrils appear concomitant with the restoration of ribosomal and ergastoplasmic morphology as early as 12 hours after administration of ascorbic acid, with complete disappearance of the scorbutic extracellular material within 24 hours. Observations of this scorbutic material do not support the concept that it is a collagen precursor.

scholarly journals COLLAGEN BIOSYNTHESIS

1957 ◽  
Vol 3 (5) ◽  
pp. 685-695 ◽  
Author(s):  
J. Frederick Woessner ◽  
Bernard S. Gould
Keyword(s):  
Ascorbic Acid ◽  
Cell Growth ◽  
Lung Tissue ◽  
Appreciable Effect ◽  
Collagen Biosynthesis ◽  
Embryonic Lung ◽  
Marked Contrast ◽  
Collagen Formation ◽  
Quantitative Studies ◽  
Total Failure

Quantitative studies of collagen formation by chick embryonic lung tissue grown in media deficient in, or completely lacking, ascorbic acid have been carried out. Cell growth and collagen formation in such cultures can proceed almost normally in media lacking ascorbic acid. Ascorbic acid in combination with whole embryo extract, dialyzed media, or synthetic mixture number 703 was found to have no appreciable effect on cell growth or total collagen formation. This is in marked contrast to the almost total failure of collagen formation in scorbutic animals and suggests that for slow collagen biosynthesis as distinct from more prolific collagen-producing systems, ascorbic acid plays an indirect role.

An Electron-Microscope Study of the in vitro Transformation of Human Leucocytes

1967 ◽  
Vol 2 (3) ◽  
pp. 359-370
Author(s):  
J. A. CHAPMAN ◽  
M. W. ELVES ◽  
J. GOUGH
Keyword(s):  
Endoplasmic Reticulum ◽  
Electron Microscope ◽  
Messenger Rna ◽  
Human Peripheral Blood ◽  
Limited Extent ◽  
Single Particles ◽  
Blast Cells ◽  
Protein Secreting

Electron-microscope studies of cultured small lymphocytes from human peripheral blood transforming into larger blastoid cells in the presence of phytohaemagglutinin (PHA) show that the transformed cell possesses the preliminary stages of development of a protein-synthesizing system. The transformed blastoid cell has abundant ribosomes, although, in contrast with in vivo protein-secreting cells, many of these occur as single particles with only a small proportion Linked in polysomal clusters. Endoplasmic reticulum membranes occur to a very limited extent and with a marked paucity of attached ribosomal particles; the few attached particles are usually located in groups. Some endoplasmic reticulum membranes revealed degenerative changes in otherwise normal cells. A moderately well-developed Golgi apparatus was a characteristic feature of the cells. Apart from the relatively low proportion of polysomes, in vitro PHA-transformed blastoid cells are identical in fine structure to in vivo blast cells (otherwise known as immunoblasts, haemocytoblasts, etc.) occurring in the immune response. It is suggested that messenger-RNA production in PHA-stimulated transformed cells may be reduced and that this could explain the limited number of polysomes and the restricted development of the endoplasmic reticulum.

scholarly journals Transient Cerebral Ischemia Activates Processing of xbp1 Messenger RNA Indicative of Endoplasmic Reticulum Stress

2003 ◽  
Vol 23 (4) ◽  
pp. 449-461 ◽  
Author(s):  
Wulf Paschen ◽  
Christoph Aufenberg ◽  
Svenja Hotop ◽  
Thorsten Mengesdorf
Keyword(s):  
Endoplasmic Reticulum ◽  
Cerebral Ischemia ◽  
Er Stress ◽  
Messenger Rna ◽  
Stress Proteins ◽  
Focal Cerebral Ischemia ◽  
Signal Transduction Pathway ◽  
Transient Cerebral Ischemia ◽  
Mrna Levels ◽  
Xbp1 Mrna

Cells respond to conditions associated with endoplasmic reticulum (ER) dysfunction with activation of the unfolded protein response, characterized by a shutdown of translation and induction of the expression of genes coding for ER stress proteins. The genetic response is based on IRE1-induced processing of xbp1 messenger RNA (mRNA), resulting in synthesis of new XBP1proc protein that functions as a potent transcription factor for ER stress genes. xbp1 processing in models of transient global and focal cerebral ischemia was studied. A marked increase in processed xbp1 mRNA levels during reperfusion was observed, most pronounced (about 35-fold) after 1-h occlusion of the right middle cerebral artery. The rise in processed xbp1 mRNA was not paralleled by a similar increase in XBP1proc protein levels because transient ischemia induces severe suppression of translation. As a result, mRNA levels of genes coding for ER stress proteins were only slightly increased, whereas mRNA levels of heat-shock protein 70 rose about 550-fold. Under conditions associated with ER dysfunction, cells require activation of the entire ER stress-induced signal transduction pathway, to cope with this severe form of stress. After transient cerebral ischemia, however, the block of translation may prevent synthesis of new XBP1proc protein and thus hinder recovery from ischemia-induced ER dysfunction.

scholarly journals Endoplasmic Reticulum Stress Is Involved in Baicalin Protection on Chondrocytes From Patients With Osteoarthritis

Dose-Response ◽  
2018 ◽  
Vol 16 (4) ◽  
pp. 155932581881063 ◽  
Author(s):  
Jiangang Cao ◽  
Yu Zhang ◽  
Tianyi Wang ◽  
Bo Li
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Viability ◽  
Er Stress ◽  
Messenger Rna ◽  
Cell Counting ◽  
Protective Effects ◽  
Gene Expressions ◽  
Protein Levels

Osteoarthritis (OA) affects elderly population worldwide and endoplasmic reticulum (ER) stress is known to be positively correlated with OA development. Previous reports prove the cytoprotective effects of baicalin on chondrocytes, whereas the mechanisms are hardly reported. Hence, we aimed to investigate the links between OA, ER stress, and baicalin. Chondrocytes from patients with OA were subjected to H2O2 treatment with or without baicalin pretreatment, and cell viability was assessed via Cell Counting Kit-8. Messenger RNA (mRNA) amounts of apoptosis-related genes (Bax, Bcl-2, and Caspase-3), extracellular matrix (ECM)-related genes (Collange I, Collange II, Aggrecan, and Sox9) and ER stress hallmarks (binding immunoglobulin protein [BiP] C/EBP homologous protein [CHOP]) were evaluated via quantitative real-time PCR. Bax, Bcl-2, BiP, and CHOP protein levels were analyzed via Western blot. Baicalin suppressed the changes in cell viability and apoptosis-related gene expressions caused by H2O2. Reactive oxygen species and glutathione/oxidized glutathione assay showed that H2O2 enhanced oxidative stress. Baicalin suppressed H2O2-induced downregulation of mRNA expression of ECM-related genes. Moreover, baicalin reduced H2O2-stimulated increase in oxidative stress and the expression of ER stress hallmarks. Endoplasmic reticulum stress inducer abolished the protective activities, whereas ER stress inhibitor did not exhibit extra protective effects. Baicalin pretreatment protected patient-derived chondrocytes from H2O2 through ER stress inhibition.

scholarly journals Messenger RNA targeting to endoplasmic reticulum stress signalling sites

Nature ◽  
2008 ◽  
Vol 457 (7230) ◽  
pp. 736-740 ◽  
Author(s):  
Tomás Aragón ◽  
Eelco van Anken ◽  
David Pincus ◽  
Iana M. Serafimova ◽  
Alexei V. Korennykh ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Messenger Rna ◽  
Rna Targeting ◽  
Stress Signalling

scholarly journals Direct association of messenger RNA labeled in the presence of fluoroorotate with membranes of the endoplasmic reticulum in rat liver.

1976 ◽  
Vol 70 (1) ◽  
pp. 47-58 ◽  
Author(s):  
J Cardelli ◽  
B Long ◽  
H C Pitot
Keyword(s):  
Endoplasmic Reticulum ◽  
Ribosomal Rna ◽  
Messenger Rna ◽  
Translational Regulation ◽  
Orotic Acid ◽  
Complete Removal ◽  
High Ionic Strength ◽  
Messenger Rnas ◽  
Direct Association ◽  
Pancreatic Rnase

Liver rough endoplasmic reticulum (RER) membranes were isolated from rats given [3H]orotic acid for 48 h (ribosomal RNA [rRNA] label) or for 3 h along with 5-fluoroorotate; this latter procedure permits the labeling of cytoplasmic messenger RNAs (mRNAs) in the absence of rRNA labeling. More than 50% of the labeled mRNA remained attached to membranes of the RER after complete removal of ribosomes with a buffer of high ionic strength in the presence of puromycin. Under similar conditions, membranes retained 40% of their polyadenylate as determined by a [3H]-polyuridylate hybridization assay. Treatment of mRNA-labeled endoplasmic reticulum membranes with pancreatic RNase indicates that the polyadenylate and possibly nonpolyadenylate-pyrimidine portions of the messenger are involved in the binding of mRNA to the membranes. The implication of these results in furthering our understanding of the mechanisms of the translational regulation of genetic expression is discussed.

scholarly journals Endoplasmic Reticulum Oxidative Stress Triggers Tgf-Beta-Dependent Muscle Dysfunction by Accelerating Ascorbic Acid Turnover

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Diego Pozzer ◽  
Mariagrazia Favellato ◽  
Marco Bolis ◽  
Roberto William Invernizzi ◽  
Francesca Solagna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Ascorbic Acid ◽  
Muscle Dysfunction ◽  
Tgf Beta

Ultrastructural changes accompany inhibition of proteoglycan synthesis in chondrocytes by Cyclofenil diphenol

1989 ◽  
Vol 92 (2) ◽  
pp. 271-280 ◽  
Author(s):  
C.A. Lancaster ◽  
P.R. Fryer ◽  
S. Griffiths ◽  
R.M. Mason
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Electron Density ◽  
Lipid Droplets ◽  
Secretory Pathway ◽  
Ultrastructural Changes ◽  
Proteoglycan Synthesis ◽  
Filamentous Material

Cyclofenil diphenol, a weak non-steroidal oestrogen, profoundly inhibits [35S]proteoglycan synthesis in cultures of Swarm chondrosarcoma chondrocytes under conditions in which protein synthesis is only marginally reduced. In the present experiments it was shown that after a 40-min treatment with Cyclofenil diphenol (90 micrograms ml-1) most of the normally abundant Golgi stacks in these cells disappeared and after 60 min they were absent. After 2–3 h treatment the cisternae of the endoplasmic reticulum (ER) were grossly distended and transformed into large ribosome-studded vesicles containing flocculent and filamentous material. These changes were dependent on the concentration of Cyclofenil and were fully reversible within 21 h of withdrawing the drug. The ultrastructural changes differed in some aspects if protein synthesis was blocked with cycloheximide for 15 min or 180 min before and during treatment with Cyclofenil. The Golgi disappeared but the ER cisternae, though distended, formed a continuous network and swollen ribosome-studded vesicles did not develop. However, non-membrane-bounded structures containing lipid droplets and material of low electron density developed in the cytoplasm under these conditions. The ultrastructural changes induced by Cyclofenil differ from those induced by monensin and diethylcarbamazine, suggesting that the drug acts at a different point in the secretory pathway for macromolecules.

Cellular functions of ascorbic acid

1990 ◽  
Vol 68 (10) ◽  
pp. 1166-1173 ◽  
Author(s):  
Harish Padh
Keyword(s):  
Ascorbic Acid ◽  
Reduced Form ◽  
Enzymatic Reactions ◽  
Cellular Functions ◽  
Animal Cells ◽  
Major Function ◽  
Collagen Formation ◽  
Oxidative Products ◽  
Catalytic Cycles

It has long been suspected that ascorbic acid is involved in many cellular reactions. This is evident from the multitude of seemingly unrelated symptoms seen in scurvy. However, until recently, our understanding of its involvement was confined to its role in the synthesis of collagen. Studies in the past few years have unveiled mechanisms of its actions in collagen formation and many other enzymatic reactions. In addition, numerous physiological responses are reportedly affected by ascorbic acid. From the well-characterized enzymatic reactions involving ascorbic acid, it has become clear that in animal cells the ascorbate does not seem to be directly involved in catalytic cycles. Rather its major function seems to keep prosthetic metal ions in their reduced form. The role of ascorbate as a reductant in these enzymatic reactions complements its other antioxidant functions which have been recently appreciated, including that as a scavenger of free radicals. Therefore, it seems that the major function of ascorbate is to protect tissues from harmful oxidative products and to keep certain enzymes in their required reduced forms. However, it remains unclear how the deficiency of ascorbate leads to the pathological symptoms found in scurvy.Key words: ascorbic acid, vitamin C, biochemical functions, antioxidant, recommended dietary allowances, hydroxylation.

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