Nuclear factor I-B (Nfib) deficient mice have severe lung hypoplasia

Gründer, Albert; Ebel, Thorsten T.; Mallo, Moisés; Schwarzkopf, Georg; Shimizu, Takehiko; Sippel, Albrecht E.; Schrewe, Heinrich

doi:10.1016/s0925-4773(01)00640-2

Cited by 99 publications

(102 citation statements)

References 49 publications

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“…Nfib ‐deficient mice possess unique defects in lung maturation; Nfib null mice develop severely delayed lung development and die at birth (Grunder et al. 2002) with Nfib hemizygous mice surviving beyond 24 h of birth (Grunder et al. 2002; Steele‐Perkins et al.…”

Section: Discussionmentioning

confidence: 99%

“…2005), and Nfib ‐deficient (−/−) animals show defects in lung development and die at birth with immature lungs (Grunder et al. 2002; Steele‐Perkins et al. 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Lung maturity is delayed in both Nfib (−/+) hemizygous and homozygous (−/−) mice, but to a different extent (Grunder et al. 2002; Steele‐Perkins et al. 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Nfib null mice die within 24 h of birth, and 60% of Nfib hemizygous newborns survive past 24 h of age (Grunder et al. 2002). This suggests that loss of the Nfib gene (either one or both alleles) leads to delay in lung maturation and reduced survival after birth, and the hemizygous survivors offer an opportunity for further study.…”

Section: Introductionmentioning

confidence: 99%

“…Lungs of Nfib hemizygous mice demonstrate definite histologic evidence of delayed lung development in the late canalicular stage at E18.5, with only focal transitions to the terminal sac stage (Grunder et al. 2002) with a decrease in type I and type II cell differentiation (Steele‐Perkins et al. 2005).…”

Section: Introductionmentioning

confidence: 99%

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Nfib hemizygous mice are protected from hyperoxic lung injury and death

et al. 2017

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Nuclear Factor I (Nfi) genes encode transcription factors essential for the development of organ systems including the lung. Nfib null mice die at birth with immature lungs. Nfib hemizygous mice have reduced lung maturation with decreased survival. We therefore hypothesized that these mice would be more sensitive to lung injury and would have lower survival to hyperoxia. Adult Nfib hemizygous mice and their wild‐type (Wt) littermates were exposed to 100% O2 for 89, 80, 72 and 66 h for survival studies with lung outcome measurements at 66 h. Nfib hemizygous and Wt controls were also studied in RA at 66 h. Cell counts and cytokines were measured in bronchoalveolar lavage (BAL); lung sections examined by histopathology; lung angiogenic and oxidative stress gene expression assessed by real‐time PCR. Unexpectedly, Nfib hemizygous mice (0/14–0%) had significantly lower mortality compared to Wt mice (10/22–45%) at 80 h of hyperoxia (P < 0.003). LD 50 was 80 h in the Wt group versus 89 h in the hemizygous group. There were no differences in BAL cell counts between the groups. Among the cytokines studied, MIP‐2 was significantly lower in hemizygous mice exposed to hyperoxia. New vessel formation, edema, congestion, and alveolar hemorrhage were noted on histopathology at 72 and 80 h in wild‐type mice. Nfib hemizygous lungs had significant downregulation of genes involved in redox signaling and inflammatory pathways. Adult Nfib hemizygous mice are relatively resistant to hyperoxia compared to wild‐type littermates. Mechanisms contributing to this resistance are not clear; however, transcription factors such as Nfib may regulate cell survival and play a role in modulating postnatal lung development.

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Section: Discussionmentioning

confidence: 99%

“…2005), and Nfib ‐deficient (−/−) animals show defects in lung development and die at birth with immature lungs (Grunder et al. 2002; Steele‐Perkins et al. 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Lung maturity is delayed in both Nfib (−/+) hemizygous and homozygous (−/−) mice, but to a different extent (Grunder et al. 2002; Steele‐Perkins et al. 2005).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nfib hemizygous mice are protected from hyperoxic lung injury and death

et al. 2017

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Prognostic significance of NFIA and NFIB in esophageal squamous carcinoma and esophagogastric junction adenocarcinoma

Yang

Zhou

Chen³

et al. 2018

Cancer Medicine

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The nuclear factor I (NFI) family members, especially NFIA and NFIB, play essential roles in cancers. The roles of NFIA and NFIB in esophageal squamous cell carcinoma (ESCC) and esophagogastric junction adenocarcinoma (EJA) remain poorly known. This study aimed to determine the expression of NFIA and NFIB in ESCC and EJA and elucidate their prognostic significance. The expression of NFIA and NFIB was examined in 163 ESCC samples and 26 EJA samples by immunohistochemistry. The results showed that high NFIA expression correlated significantly with poor differentiation, lymph node metastasis, and advanced TNM stage in patients with ESCC. High NFIB expression only correlated with poor differentiation in patients with ESCC. Survival analysis showed that NFIA but not NFIB associated with short overall survival (OS) and disease‐free survival (DFS) of patients with ESCC. On the other hand, high NFIB expression correlated with lymph node metastasis, advanced TNM stage, and short OS and DFS in patients with EJA. Finally, multivariate analysis demonstrated that high NFIA expression was an independent prognostic factor for ESCC. Taken together, these results demonstrated that NFIA and NFIB could serve as prognostic indicators for ESCC and EJA, respectively.

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Absence of the transcription factor Nfib delays the formation of the basilar pontine and other mossy fiber nuclei

Kumbasar

Plachez

Gronostajski

et al. 2008

J of Comparative Neurology

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Transcription factors of the Nuclear Factor I (Nfi) family are important for the development of specific neuronal and glial populations in the nervous system. One such population, the neurons of the basilar pontine nuclei, expresses high levels of Nfi proteins, and the pontine nuclei are greatly reduced in mice lacking a functional Nfib gene. Pontine neurons, along with other precerebellar neurons that populate the hindbrain, arise from precursors in the lower rhombic lip and migrate anteroventrally to reach their final location. Using immunohistochemistry, we find that NFI-B expression is specific for mossy fiber populations of the precerebellar system. Analysis of the Nfib ؊/؊ hindbrain indicates that the development of the basilar pontine nuclei is delayed, with pontine neurons migrating 1-2 days later than in control animals, and that significantly fewer pontine neurons are produced. While the mossy fiber nuclei of the caudal medulla do form, they also exhibit a developmental delay. Indexing terms: precerebellar; mossy fiber; cell migration; neurogenesis; hindbrain The mature brain is composed of many subclasses of neurons and glia, each of which acquires a unique identity during development. Such identity is conferred by transcription factors that work alone or in combination to determine cell fate. One set of transcription factors that is critical for the development of specific subpopulations of both neurons and glia in the nervous system are the Nuclear Factor I (Nfi) transcription factors, a family consisting of Nfia, Nfib, Nfic, and Nfix (for a general review, see Gronostajski, 2000). Additional diversity in this set of factors is generated by alternative splicing, resulting in several possible isoforms for each protein.

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Nuclear factor I-B (Nfib) deficient mice have severe lung hypoplasia

Cited by 99 publications

References 49 publications

Nfib hemizygous mice are protected from hyperoxic lung injury and death

Nfib hemizygous mice are protected from hyperoxic lung injury and death

Prognostic significance of NFIA and NFIB in esophageal squamous carcinoma and esophagogastric junction adenocarcinoma

Absence of the transcription factor Nfib delays the formation of the basilar pontine and other mossy fiber nuclei

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