Mast Cell Proliferation in Adult Mice

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19–48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30–500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.

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Mucosal mast cell proliferation following normal and heterotopic infections of the nematodeNippostrongylus brasiliensisin rats

Apmis ◽

10.1111/j.1699-0463.1994.tb05208.x ◽

1994 ◽

Vol 102 (7-12) ◽

pp. 589-596 ◽

Cited By ~ 8

Author(s):

NAOKI ARIZONO ◽

MINORU YAMADA ◽

TATSUYA TEGOSHI ◽

MANABU OKADA ◽

RYUICHI UCHIKAWA ◽

...

Keyword(s):

Cell Proliferation ◽

Mast Cell ◽

Mucosal Mast Cell

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Systemic Administration of Parathyroid Hormone-Related Peptide (PTHrP) 1-36 Enhances β-Cell Proliferation and Increases β-Cell Mass in Adult Mice.

10.1210/endo-meetings.2010.part3.p10.p3-479 ◽

2010 ◽

pp. P3-479-P3-479

Author(s):

KR Williams ◽

DK Abanquah ◽

SJ Gokhale ◽

H Lin ◽

NK Guthalu ◽

...

Keyword(s):

Cell Proliferation ◽

Parathyroid Hormone ◽

Cell Mass ◽

Systemic Administration ◽

Β Cell ◽

Related Peptide ◽

Adult Mice ◽

Parathyroid Hormone Related Peptide

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Partial Hearing Restoration after ERBB2 Induction in Deafened Adult Mice

10.1101/838649 ◽

2019 ◽

Author(s):

Jingyuan Zhang ◽

Daxiang Na ◽

Miriam Dilts ◽

Kenneth S. Henry ◽

Patricia M. White

Keyword(s):

Cell Proliferation ◽

Hearing Loss ◽

Noise Exposure ◽

Supporting Cell ◽

Supporting Cells ◽

Adult Mice ◽

Hearing Thresholds ◽

Brainstem Response ◽

Noise Damage ◽

Cochlear Supporting Cells

AbstractNoise induced hearing loss (NIHL) affects over ten million adults in the United States, and there is no biological treatment to restore endogenous function after damage. We hypothesized that activation of signaling from ERBB2 receptors in cochlear supporting cells could mitigate NIHL damage. We used the Tet-On genetic expression system to drive a constitutively active variant of ERBB2 (CA-ERBB2) in cochlear supporting cells three days after permanent noise damage in young adult mice. Hearing thresholds were assessed with auditory brainstem response tests prior to noise damage, and hearing recovery was assessed over a three month period. We evaluated supporting cell proliferation, inner and outer hair cell (IHC and OHC) survival, synaptic preservation, and IHC cytoskeletal alterations with histological techniques. Mice harboring CA-ERBB2 capability had similar hearing thresholds to control littermates prior to and immediately after noise exposure, and incurred similar levels of permanent hearing loss. Two and three months after noise exposure, CA-ERBB2+ mice demonstrated a partial but significant reversal of NIHL threshold shifts at the lowest frequency tested, out of five frequencies (n=19 total mice, p=0.0015, ANOVA). We also observed improved IHC and OHC survival (n=7 total cochleae, p=5 × 10−5, Kruskal-Wallis rank sum test). There was no evidence for sustained supporting cell proliferation. Some mortality was associated with doxycycline and furosemide treatments to induce the Tet-ON system. These data suggest that ERBB2 signaling in supporting cells promotes HC repair and some functional recovery. Funded by NIH R01 DC014261, and grants from the Schmitt Foundation and UR Ventures.

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The gene coding for a major tumor rejection antigen of tumor P815 is identical to the normal gene of syngeneic DBA/2 mice.

Journal of Experimental Medicine ◽

10.1084/jem.173.6.1373 ◽

1991 ◽

Vol 173 (6) ◽

pp. 1373-1384 ◽

Cited By ~ 204

Author(s):

B Van den Eynde ◽

B Lethé ◽

A Van Pel ◽

E De Plaen ◽

T Boon

Keyword(s):

Mast Cell ◽

Tumor Rejection ◽

Cosmid Library ◽

Adult Mice ◽

Gene Coding ◽

Tumor Rejection Antigen ◽

Normal Gene ◽

Mast Cell Line ◽

High Level

We showed previously that mouse mastocytoma P815 expresses several distinct antigens that are recognized by cytolytic T lymphocytes (CTL) of syngeneic DBA/2 mice. Antigens P815A and P815B are usually lost jointly and are targets for immune rejection responses in vivo. We used a cosmid library and a CTL stimulation assay to obtain transfectants expressing tumor rejection antigen P815A. From these transfectants we retrieved gene P1A which transferred the expression of both P815A and B. This gene is unrelated to three previously isolated genes coding for tum-antigens. It encodes a putative protein of 224 amino acids which contains two highly acidic domains showing homology with similar regions of nuclear proteins. The P1A gene expressed by tumor P815 is completely identical to the gene present in normal DBA/2 cells. Expression of the gene was tested by Northern blots. Cells from liver, spleen, and a number of mast cell lines were negative, but mast cell line L138.8A produced a high level of P1A message and was lysed by CTL directed against antigens P815A and B. We conclude that major tumor rejection antigens of P815 are encoded by a gene showing little or no expression in most normal cells of adult mice.

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