Keratinocyte growth factor accelerates compensatory growth in the remaining lung after trilobectomy in rats

Matsumoto, Keitaro; Nagayasu, Takeshi; Hishikawa, Yoshitaka; Tagawa, Tetsuzo; Yamayoshi, Takatomo; Abo, Takafumi; Tobinaga, Shuichi; Furukawa, Kaori; Koji, Takehiko

doi:10.1016/j.jtcvs.2008.11.037

Cited by 26 publications

(31 citation statements)

References 22 publications

(18 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Changes in lung weight index, lung volume index as well as morphometric parameters were accompanied by a significant increase in pulmonary cell proliferation index, providing the first evidence for a role of KGF in CLG . A more recent study corroborated our findings where epithelial cell proliferation was further enhanced after in vivo transfection of a KGF cDNA vector in a model of CLG in rats, confirming KGF as an important lung mitogenic factor (Matsumoto, et al, 2009). …”

Section: Keratinocyte Growth Factor-i (Kgf)supporting

confidence: 88%

Compensatory Lung Growth After Pneumonectomy

Fernández¹,

Isbell²,

Jones³

et al. 2012

Topics in Thoracic Surgery

View full text Add to dashboard Cite

Section: Keratinocyte Growth Factor-i (Kgf)supporting

confidence: 88%

Compensatory Lung Growth After Pneumonectomy

Fernández¹,

Isbell²,

Jones³

et al. 2012

Topics in Thoracic Surgery

View full text Add to dashboard Cite

“…ERK1/2 is a major transducer of extracellular proliferation signals and is responsible for transferring these signals to downstream nuclear effectors of cellular proliferation. ERK1/2 responds upstream to epidermal growth factor receptor signaling and targets PCNA downstream, both of which proliferative markers have been shown to be strongly upregulated following PNX (21,41). Other early response genes are upregulated immediately following PNX, including Egr-1 and TTF-1 (Nkx2.1), the latter of which is a critical factor in lung development (31,43,56).…”

Section: Discussionmentioning

confidence: 99%

Partial pneumonectomy of telomerase null mice carrying shortened telomeres initiates cell growth arrest resulting in a limited compensatory growth response

Jackson

Lee

Reddy

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Telomerase mutations and significantly shortened chromosomal telomeres have recently been implicated in human lung pathologies. Natural telomere shortening is an inevitable consequence of aging, which is also a risk factor for development of lung disease. However, the impact of shortened telomeres and telomerase dysfunction on the ability of lung cells to respond to significant challenge is still largely unknown. We have previously shown that lungs of late generation, telomerase null B6.Cg- Terc tm1Rdp mice feature alveolar simplification and chronic stress signaling at baseline, a phenocopy of aged lung. To determine the role telomerase plays when the lung is challenged, B6.Cg- Terc tm1Rdp mice carrying shortened telomeres and wild-type controls were subjected to partial pneumonectomy. We found that telomerase activity was strongly induced in alveolar epithelial type 2 cells (AEC2) of the remaining lung immediately following surgery. Eighty-six percent of wild-type animals survived the procedure and exhibited a burst of early compensatory growth marked by upregulation of proliferation, stress response, and DNA repair pathways in AEC2. In B6.Cg- Terc tm1Rdp mice carrying shortened telomeres, response to pneumonectomy was characterized by decreased survival, diminished compensatory lung growth, attenuated distal lung progenitor cell response, persistent DNA damage, and cell growth arrest. Overall, survival correlated strongly with telomere length. We conclude that functional telomerase and properly maintained telomeres play key roles in both long-term survival and the early phase of compensatory lung growth following partial pneumonectomy.

show abstract

“…The best results were obtained with 6 pulses of 50 V for 80 ms, each separated by 1.0 s, which were delivered by electrode disks (data not shown). The SD rat was anesthetized with pentobarbital, then Flag-hKGF DNA plasmid driven by a CMV14 promoter that cording region was kindly provided by Dr. Jeffrey Rubin from the National Cancer Institute, (Bethesda, MD, USA) [15] was injected at 50 lg into the epithelial lesion of right external auditory canal (EAC), and electric pulses were administered once (short-term model) or injected five times every fourth day (long-term model). For the left ear, a Flag-plasmid driven by a CMV14 promoter (Sigma, MO, USA) was injected and used as control.…”

Section: Electroporation For Kgf Cdna In Vivomentioning

confidence: 99%

In vivo over-expression of KGF mimic human middle ear cholesteatoma

Yamamoto‐Fukuda

Akiyama

Shibata

et al. 2014

Eur Arch Otorhinolaryngol

Self Cite

View full text Add to dashboard Cite

We reported previously that keratinocyte growth factor (KGF), a mesenchymal cell-derived paracrine growth factor, plays an important role in middle ear cholesteatoma formation, which is characterized by marked proliferation of epithelial cells. Here, we investigated whether KGF, the main factor that induces cholesteatoma, overexpression in vivo results in the formation of cholesteatoma. Flag-hKGF cDNA driven by CMV14 promoter was transfected through electroporation into the external auditory canal (EAC) of rats once (short-term model) or five times on every fourth day (long-term model). Ears transfected with empty vector were used as controls. Successful transfection of plasmids into epithelial and stromal cells was confirmed by Flag immunohistochemistry. In the short-term model, the intensity of KGF protein was the strongest in hKGF transfected ear at day 4. KGF expression induced epithelial cell proliferation, reaching a peak level at day 4 and then decreased later, while in the long-term model, KGF expression in the EAC led to middle ear cholesteatoma formation. In conclusion, we described here a new experimental model of human middle ear cholesteatoma, and demonstrated that KGF and KGF receptor paracrine action play an essential role in middle ear cholesteatoma formation in an in vivo model.

show abstract

Keratinocyte growth factor accelerates compensatory growth in the remaining lung after trilobectomy in rats

Cited by 26 publications

References 22 publications

Compensatory Lung Growth After Pneumonectomy

Compensatory Lung Growth After Pneumonectomy

Partial pneumonectomy of telomerase null mice carrying shortened telomeres initiates cell growth arrest resulting in a limited compensatory growth response

In vivo over-expression of KGF mimic human middle ear cholesteatoma

Contact Info

Product

Resources

About