scholarly journals Bony lesions in early tetrapods and the evolution of mineralized tissue repair

Paleobiology ◽  
2019 ◽  
Vol 45 (4) ◽  
pp. 676-697 ◽  
Author(s):  
Eva C. Herbst ◽  
Michael Doube ◽  
Timothy R. Smithson ◽  
Jennifer A. Clack ◽  
John R. Hutchinson
Keyword(s):  
Bone Healing ◽  
Tissue Repair ◽  
Bone Structure ◽  
Early Carboniferous ◽  
Skeletal Tissue ◽  
Mineralized Tissues ◽  
Repair Mechanisms ◽  
Evolutionary Context ◽  
Bony Lesions ◽  
Early Tetrapods

AbstractBone healing is an important survival mechanism, allowing vertebrates to recover from injury and disease. Here we describe newly recognized paleopathologies in the hindlimbs of the early tetrapods Crassigyrinus scoticus and Eoherpeton watsoni from the early Carboniferous of Cowdenbeath, Scotland. These pathologies are among the oldest known instances of bone healing in tetrapod limb bones in the fossil record (about 325 Ma). X-ray microtomographic imaging of the internal bone structure of these lesions shows that they are characterized by a mass of trabecular bone separated from the shaft's trabeculae by a layer of cortical bone. We frame these paleopathologies in an evolutionary context, including additional data on bone healing and its pathways across extinct and extant sarcopterygians. These data allowed us to synthesize information on cell-mediated repair of bone and other mineralized tissues in all vertebrates, to reconstruct the evolutionary history of skeletal tissue repair mechanisms. We conclude that bone healing is ancestral for sarcopterygians. Furthermore, other mineralized tissues (aspidin and dentine) were also capable of healing and remodeling early in vertebrate evolution, suggesting that these repair mechanisms are synapomorphies of vertebrate mineralized tissues. The evidence for remodeling and healing in all of these tissues appears concurrently, so in addition to healing, these early vertebrates had the capacity to restore structure and strength by remodeling their skeletons. Healing appears to be an inherent property of these mineralized tissues, and its linkage to their remodeling capacity has previously been underappreciated.

scholarly journals Osteogenic protein-1 mRNA expression is selectively modulated after acute ischemic renal injury.

1998 ◽  
Vol 9 (8) ◽  
pp. 1456-1463
Author(s):  
M M Almanzar ◽  
K S Frazier ◽  
P H Dube ◽  
A I Piqueras ◽  
W K Jones ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Renal Injury ◽  
Tissue Repair ◽  
Western Blots ◽  
Time Points ◽  
Mrna Content ◽  
Repair Mechanisms ◽  
Osteogenic Protein ◽  
Ischemic Renal Injury ◽  
Deficient Mice

Osteogenic protein-1 (OP-1) is a morphogenetic factor highly expressed in the kidney and involved in tissue repair and development. Homozygous OP-1-deficient mice die shortly after birth due mainly to arrest of renal growth and differentiation. Because postischemic injury involves several repair mechanisms, this study examined whether kidney OP-1 mRNA expression is modulated after ischemia. Acute ischemic renal injury was achieved in rats by unilateral clamping of the renal pedicle followed by reperfusion. Rats were killed at 3, 6, 12, 24, and 48 h and 7 d after reperfusion, and kidneys were microdissected and analyzed by histology and Northern and Western blots. Changes in OP-1 mRNA were determined by measuring the ratio of OP-1/glyceraldehyde 3-phosphate dehydrogenase signals for each OP-1 transcript (4.0 and 2.4 kb) from ischemic, opposite, and sham-operated rats. The OP-1 mRNA content for transcript 4.0 kb was fivefold lower in the whole ischemic kidney compared with that in sham animals 24 h after reperfusion. In the ischemic medulla, OP-1 mRNA was strikingly downregulated 20-fold when compared with the ischemic cortex. Results for transcript 2.4 kb and for the other time points were comparable. OP-1 mRNA expression was also affected in the opposite medulla compared with the sham medulla. However, only in the ischemic medulla was the relative OP-1 content significantly lower at all time points. Similar results were obtained when analyzing OP-1 protein by Western blot at 24 h after reperfusion. Seven days after reperfusion, the levels of OP-1 mRNA returned to baseline. In conclusion, kidney OP-1 mRNA and protein are selectively downregulated in the medulla after acute ischemic renal injury. OP-1 modulation may be a key element for kidney repair.

Stem Cells and Their Use in Skeletal Tissue Repair

2010 ◽  
pp. 103-124
Author(s):  
Laura Baumgartner ◽  
Vuk Savkovic ◽  
Susanne Trettner ◽  
Colette Martin ◽  
Nicole I. zur Nieden
Keyword(s):  
Stem Cells ◽  
Tissue Repair ◽  
Skeletal Tissue

Evaluation of skeletal tissue repair, Part 2: Enhancement of skeletal tissue repair through dual-growth-factor-releasing hydrogels within an ex vivo chick femur defect model

2014 ◽  
Vol 10 (10) ◽  
pp. 4197-4205 ◽  
Author(s):  
E.L. Smith ◽  
J.M. Kanczler ◽  
D. Gothard ◽  
C.A. Roberts ◽  
J.A. Wells ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tissue Repair ◽  
Ex Vivo ◽  
Defect Model ◽  
Skeletal Tissue

scholarly journals Locomotory behaviour of early tetrapods from Blue Beach, Nova Scotia, revealed by novel microanatomical analysis

2021 ◽  
Vol 8 (5) ◽  
pp. 210281
Author(s):  
Kendra I. Lennie ◽  
Sarah L. Manske ◽  
Chris F. Mansky ◽  
Jason S. Anderson
Keyword(s):  
Nova Scotia ◽  
Fossil Record ◽  
Early Carboniferous ◽  
Late Devonian ◽  
Ground Reaction Forces ◽  
Limb Bones ◽  
Additional Information ◽  
Reaction Forces ◽  
Early Tetrapods ◽  
Locomotory Behaviour

Evidence for terrestriality in early tetrapods is fundamentally contradictory. Fossil trackways attributed to early terrestrial tetrapods long predate the first body fossils from the Late Devonian. However, the Devonian body fossils demonstrate an obligatorily aquatic lifestyle. Complicating our understanding of the transition from water to land is a pronounced gap in the fossil record between the aquatic Devonian taxa and presumably terrestrial tetrapods from the later Early Carboniferous. Recent work suggests that an obligatorily aquatic habit persists much higher in the tetrapod tree than previously recognized. Here, we present independent microanatomical data of locomotor capability from the earliest Carboniferous of Blue Beach, Nova Scotia. The site preserves limb bones from taxa representative of Late Devonian to mid-Carboniferous faunas as well as a rich trackway record. Given that bone remodels in response to functional stresses including gravity and ground reaction forces, we analysed both the midshaft compactness profiles and trabecular anisotropy, the latter using a new whole bone approach. Our findings suggest that early tetrapods retained an aquatic lifestyle despite varied limb morphologies, prior to their emergence onto land. These results suggest that trackways attributed to early tetrapods be closely scrutinized for additional information regarding their creation conditions, and demand an expansion of sampling to better identify the first terrestrial tetrapods.

scholarly journals In vivo sequestration of innate small molecules to promote bone healing

2019 ◽  
Author(s):  
Yuze Zeng ◽  
Yu-Ru V. Shih ◽  
Gurpreet S. Baht ◽  
Shyni Varghese
Keyword(s):  
Small Molecules ◽  
Human Body ◽  
Tissue Repair ◽  
Physiological Level ◽  
Extracellular Adenosine ◽  
Injury Site ◽  
Synthetic Biomaterial ◽  
Repair Mechanisms

AbstractApproaches that enable innate repair mechanisms hold great potential for tissue repair. Herein, we describe biomaterial-assisted sequestration of small molecules to localize pro-regenerative signaling at the injury site. Specifically, we designed a synthetic biomaterial containing boronate molecules to sequester adenosine, a small molecule ubiquitously present in the human body. The biomaterial-assisted sequestration of adenosine leverages the transient surge of extracellular adenosine following injury to prolong local adenosine signaling. We demonstrated that implantation of the biomaterial patch following injury establishes an in-situ stockpile of adenosine, resulting in accelerated healing by promoting both osteoblastogenesis and angiogenesis. The adenosine content within the patch recedes to the physiological level as the tissue regenerates. In addition to sequestering endogenous adenosine, the biomaterial is also able to deliver exogenous adenosine to the site of injury, offering a versatile solution to utilizing adenosine as a potential therapeutic for tissue repair.

scholarly journals Advances in biomineralization-inspired materials for hard tissue repair

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Shuxian Tang ◽  
Zhiyun Dong ◽  
Xiang Ke ◽  
Jun Luo ◽  
Jianshu Li
Keyword(s):  
Tissue Repair ◽  
Bone Repair ◽  
Hierarchical Structures ◽  
Hard Tissue ◽  
Future Directions ◽  
Artificial Materials ◽  
Mineral Phases ◽  
Different Types ◽  
Mineralized Tissues ◽  
Underlying Mechanisms

AbstractBiomineralization is the process by which organisms form mineralized tissues with hierarchical structures and excellent properties, including the bones and teeth in vertebrates. The underlying mechanisms and pathways of biomineralization provide inspiration for designing and constructing materials to repair hard tissues. In particular, the formation processes of minerals can be partly replicated by utilizing bioinspired artificial materials to mimic the functions of biomolecules or stabilize intermediate mineral phases involved in biomineralization. Here, we review recent advances in biomineralization-inspired materials developed for hard tissue repair. Biomineralization-inspired materials are categorized into different types based on their specific applications, which include bone repair, dentin remineralization, and enamel remineralization. Finally, the advantages and limitations of these materials are summarized, and several perspectives on future directions are discussed.

Skeletal tissue regulation by catalase overexpression in mitochondria

2020 ◽  
Vol 319 (4) ◽  
pp. C734-C745 ◽  
Author(s):  
Ann-Sofie Schreurs ◽  
Samantha Torres ◽  
Tiffany Truong ◽  
Eric L. Moyer ◽  
Akhhilesh Kumar ◽  
...  
Keyword(s):  
Bone Growth ◽  
Bone Structure ◽  
Ex Vivo ◽  
Osteoclast Differentiation ◽  
Colony Growth ◽  
Activity Levels ◽  
Radial Expansion ◽  
Skeletal Tissue ◽  
Mitochondrial Ros ◽  
Hind Limb Unloading

Accumulation of oxidative damage from excess reactive oxygen species (ROS) may contribute to skeletal aging and mediate adverse responses to physiological challenges. Wild-type (WT) mice and transgenic mice (male, 16 wk of age) with human catalase targeted to the mitochondria (mCAT) were analyzed for skeletal responses to the remodeling stimuli of combined hind-limb unloading and exposure to ionizing radiation (137Cs, 2 Gy). Treatment for 2 wk caused lipid peroxidation in the bones WT but not mCAT mice, showing that transgene expression mitigated oxidative stress. Ex vivo osteoblast colony growth rate was 95% greater in mCAT than WT mice and correlated with catalase activity levels ( P < 0.005, r = 0.67), although terminal osteoblast and osteoclast differentiation were unaffected. mCAT mice had lower cancellous bone volume and cortical size than WT mice. Ambulatory control mCAT animals also displayed reduced cancellous and cortical structural properties compared with control WT mice. In mCAT but not WT mice, treatment caused an unexpectedly rapid radial expansion (+8% cortical area, +22% moment of inertia), reminiscent of compensatory bone growth during advancing age. In contrast, treatment caused similar structural deficits in cancellous tissue of mCAT and WT mice. In sum, mitochondrial ROS signaling via H2O2 was important for the acquisition of adult bone structure and catalase overexpression failed to protect cancellous tissue from treatment. In contrast, catabolic stimuli caused radial expansion in mCAT not WT mice, suggesting that mitochondrial ROS in skeletal cells act to suppress tissue turnover in response to remodeling challenges.

scholarly journals Tetrapod-like axial regionalization in an early ray-finned fish

2012 ◽  
Vol 279 (1741) ◽  
pp. 3264-3271 ◽  
Author(s):  
Lauren Cole Sallan
Keyword(s):  
Weight Bearing ◽  
Expression Patterns ◽  
Early Carboniferous ◽  
Alternative Scenario ◽  
Walking Gait ◽  
Pelvic Area ◽  
Early Tetrapods ◽  
Primitive State ◽  
Functional Explanations

Tetrapods possess up to five morphologically distinct vertebral series: cervical, thoracic, lumbar, sacral and caudal. The evolution of axial regionalization has been linked to derived Hox expression patterns during development and the demands of weight-bearing and walking on land. These evolutionary and functional explanations are supported by an absence of similar traits in fishes, living and extinct. Here, I show that, Tarrasius problematicus , a marine ray-finned fish from the Mississippian (Early Carboniferous; 359–318 Ma) of Scotland, is the first non-tetrapod known to possess tetrapod-like axial regionalization. Tarrasius exhibits five vertebral regions, including a seven-vertebrae ‘cervical’ series and a reinforced ‘sacrum’ over the pelvic area. Most vertebrae possess processes for intervertebral contact similar to tetrapod zygapophyses. The fully aquatic Tarrasius evolved these morphologies alongside other traits convergent with early tetrapods, including a naked trunk, and a single median continuous fin. Regional modifications in Tarrasius probably facilitated pelagic swimming , rather than a terrestrial lifestyle or walking gait, presenting an alternative scenario for the evolution of such traits in tetrapods. Axial regionalization in Tarrasius could indicate tetrapod-like Hox expression patterns, possibly representing the primitive state for jawed vertebrates. Alternately, it could signal a weaker relationship, or even a complete disconnect, between Hox expression domains and vertebrate axial plans.

Monocyte function and trafficking in cardiovascular disease

2012 ◽  
Vol 108 (11) ◽  
pp. 804-811 ◽  
Author(s):  
Evangelia Pardali ◽  
Johannes Waltenberger
Keyword(s):  
Cardiovascular Diseases ◽  
Tissue Repair ◽  
Vascular Diseases ◽  
Immune Defense ◽  
Injury Repair ◽  
Disease Marker ◽  
Pathological Conditions ◽  
Repair Mechanisms ◽  
Cardio Vascular

SummaryMonocytes are key effectors of the immune homeostasis and play a crucial role in (vascular) injury repair. Despite their role in immune defense and tissue repair mechanisms, monocytes are also involved in several pathological conditions such as autoimmune and cardiovascular diseases as well as cancer. This suggests that monocytes can be used as diagnostic and as therapeutic targets. A better understanding and characterisation of monocytes and their function in both physiological and pathological situations is thus of great interest. This review focuses on recent advances on the role of monocytes in cardiovascular diseases and describes the value of monocytes as either disease marker or therapeutic target for (cardio)vascular diseases.

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