Impaired wound healing in mice lacking the basement membrane protein nidogen 1

Baranowsky, Anke; Mokkapati, Sharada; Bechtel, Manuela; Krügel, Jenny; Miosge, Nicolai; Wickenhauser, Claudia; Smyth, Neil; Nischt, Roswitha

doi:10.1016/j.matbio.2009.09.004

Cited by 30 publications

(20 citation statements)

References 36 publications

(51 reference statements)

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“…DLC1 binds tensin, a membrane cytoskeletal protein, and is considered a tumor suppressor gene (66). FABP5 promotes cell proliferation (19), and NID1 is a membrane glycoprotein providing a bridge between collagen 4 and laminin with a potential role in tissue recovery (4). PDZD2 is a secreted protein and also a tumor suppressor (52,53), and it may represent a novel myokine.…”

Section: Continuedmentioning

confidence: 99%

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

Keller

Vollaard

Gustafsson

et al. 2011

Journal of Applied Physiology

213

218

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The molecular pathways that are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ∼800 gene transcripts are regulated following 6 wk of supervised endurance training in young sedentary males, referred to as the training-responsive transcriptome (TRT) (Timmons JA et al. J Appl Physiol 108: 1487-1496, 2010). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as overrepresented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9, and PAX3 were downregulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, proangiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA-level validation there were several DNA variants that associated with maximal aerobic capacity (Vo(₂max)) trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.

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Section: Continuedmentioning

confidence: 99%

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

Keller

Vollaard

Gustafsson

et al. 2011

Journal of Applied Physiology

213

218

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“…Whether this hyperproliferative phenotype would persist during further skin maturation cannot be studied owing to the perinatal lethality in this mouse strain. Interestingly, skin wounding in nidogen 1-deficient mice showed a transient delay in epidermal thinning due to hyperproliferation of basal keratinocytes in the newly formed epidermis (36). Because in these wounds, nidogen 2 deposition is unaltered when compared with control wounds, this suggests a specific role for nidogen 1, which cannot be compensated by nidogen 2.…”

Section: Discussionmentioning

confidence: 98%

Basement Membrane Deposition of Nidogen 1 but Not Nidogen 2 Requires the Nidogen Binding Module of the Laminin γ1 Chain

Mokkapati

Fleger-Weckmann

Bechtel

et al. 2011

Journal of Biological Chemistry

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The nidogen-laminin interaction is proposed to play a key role in basement membrane (BM) assembly. However, though there are similarities, the phenotypes in mice lacking nidogen 1 and 2 (nidogen double null) differ to those of mice lacking the nidogen binding module (␥1III4) of the laminin ␥1 chain. This indicates different cell-and tissue-specific functions for nidogens and their interaction with laminin and poses the question of whether the phenotypes in nidogen double null mice are caused by the loss of the laminin-nidogen interaction or rather by other unknown nidogen functions. To investigate this, we analyzed BMs, in particular those in the skin of mice lacking the nidogen binding module. In contrast to nidogen double null mice, all skin BMs in ␥1III4-deficient mice appeared normal. Furthermore, although nidogen 1 deposition was strongly reduced, nidogen 2 appeared unchanged. Mice with additional deletion of the laminin ␥3 chain, which contains a ␥1-like nidogen binding module, showed a further reduction of nidogen 1 in the dermoepidermal BM; however, this again did not affect nidogen 2. This demonstrates that in vivo only nidogen 1 deposition is critically dependent on the nidogen binding modules of the laminin ␥1 and ␥3 chains, whereas nidogen 2 is independently recruited either by binding to an alternative site on laminin or to other BM proteins.

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“…If the basement membrane is induced in amphibians before regeneration is complete, scar formation occurs and regeneration ceases [91]. The basement membrane, however, may also play a beneficial role, as wound healing is impaired in mice lacking the basement membrane component nidogen 1 [92]. Nidogens 1 and 2 are basement membrane proteins that interact with laminin, collagen IV, and perlecan.…”

Section: Mammalian Wound Healingmentioning

confidence: 99%

Regeneration and Regrowth Potentials of Digit Tips in Amphibians and Mammals

Choi¹,

Meng

Cox³

et al. 2017

International Journal of Cell Biology

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Tissue regeneration and repair have received much attention in the medical field over the years. The study of amphibians, such as newts and salamanders, has uncovered many of the processes that occur in these animals during full-limb/digit regeneration, a process that is highly limited in mammals. Understanding these processes in amphibians could shed light on how to develop and improve this process in mammals. Amputation injuries in mammals usually result in the formation of scar tissue with limited regrowth of the limb/digit; however, it has been observed that the very tips of digits (fingers and toes) can partially regrow in humans and mice under certain conditions. This review will summarize and compare the processes involved in salamander limb regeneration, mammalian wound healing, and digit regeneration in mice and humans.

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Impaired wound healing in mice lacking the basement membrane protein nidogen 1

Cited by 30 publications

References 36 publications

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

Basement Membrane Deposition of Nidogen 1 but Not Nidogen 2 Requires the Nidogen Binding Module of the Laminin γ1 Chain

Regeneration and Regrowth Potentials of Digit Tips in Amphibians and Mammals

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