Ccn1, a molecular switch that imposes a self-limiting control on inflammation and wound healing in a multitude of organs?

Weiskirchen, Ralf

doi:10.1152/ajplung.00239.2015

American Journal of Physiology-Lung Cellular and Molecular Phys

2015

DOI: 10.1152/ajplung.00239.2015

|View full text |Cite

Ccn1, a molecular switch that imposes a self-limiting control on inflammation and wound healing in a multitude of organs?

Ralf Weiskirchen

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2015

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

(1 citation statement)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TO THE EDITOR: We would like to thank Dr. Weiskirchen (5) for his interest in our recent publication (3). As we mentioned in the DISCUSSION and as pointed out by Dr. Weiskirchen, the absence of protein data in our adenovirus model represents a limitation of our study.…”

mentioning

confidence: 99%

Reply to Dr. Weiskirchen

Grazioli

Matute-Bello

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

TO THE EDITOR: We would like to thank Dr. Weiskirchen (5) for his interest in our recent publication (3). As we mentioned in the DISCUSSION and as pointed out by Dr. Weiskirchen, the absence of protein data in our adenovirus model represents a limitation of our study. Regarding the RNA expression, we also expected to find a greater difference in ccn1/cyr61 gene expression in the mice instilled with AdCyr61 compared with the control group. Although inadequate gene transfer is a possibility, we would like to point out other possibilities. The RNA was extracted from whole lung preparations. However, the adenovirus was delivered by intratracheal instillations, which result in a patchy distribution of the instillate, leaving large areas of the lung without exposure to the adenovirus. Therefore, only a portion of the measured lung was expected to show increased expression of CYR61. In addition, only the airway and alveolar epithelial cells were expected to be exposed to the adenovirus, and they represent only a fraction of the total lung cells. These two reasons would result in lower total lung expression of ccn1/cyr61, even if local expression at the target cells was robust. Further loss-of-function studies of CYR61 in the lungs will be required to confirm our results.Dr. Weiskirchen expressed a desire for additional information regarding the cloning and purification of the adenovirus. Additional details on the method we used for vector generation, cloning, and production of recombinant adenovirus can be found in the supplementary materials and methods of Ren et al.'s paper (4). For the purification process we used cesium chloride gradient ultracentrifugation as described by Chartier et al. (2). Although we agree that the presence of trace of cesium in our adenovirus cannot be completely excluded, we believe that it didn't impact our results because both adenoviruses, AdCtr and AdCyr61, were purified by the same method and we did not observe any toxic effects in the control group.Dr. Weiskirchen is interested in the weight loss we observed in the group of mice instilled with AdCyr61. Rapid weight loss is a common finding of acute lung injury models and is likely due to a combination of decreased food and water intake and increased insensible losses. Finally, we thank Dr. Weiskirchen for pointing out two mistakes regarding CYR61 definition that were made during the editing process and were not present in the submitted manuscript. Efficient generation of recombinant adenovirus vectors by homologous recombination in Escherichia coli.

show abstract

mentioning

confidence: 99%

Reply to Dr. Weiskirchen

Grazioli

Matute-Bello

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Ccn1, a molecular switch that imposes a self-limiting control on inflammation and wound healing in a multitude of organs?

Cited by 1 publication

References 9 publications

Reply to Dr. Weiskirchen

Reply to Dr. Weiskirchen

Contact Info

Product

Resources

About