8/ growth Flashcards

1
Q

what is cell hypertrophy

A
  • type of tissue growth
  • cells enlarge (without necessarily dividing)
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2
Q

what is cell proliferation

A
  • type of tissue growth
  • daughter cells half the volume, need hypertrophy to get back to same volume as parent
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3
Q

what is growth by accretion

A
  • type of tissue growth
  • cells excrete extracellular matrix around them - eg cartilage
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4
Q

cell cycle outline

A
  • G1: very long or permanent
  • S: DNA replication
  • G2: cell doesn’t function well at this stage - temp gap
  • M: nuclear and cytoplasmic division
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5
Q

cell cycle checkpoints

A
  • end of G1: start checkpoint, checks for favourable environment. activates by FGF and IGF, inhibited by TS gene Rb (mutated in retinoblastoma)
  • G2/M: enter mitosis. check for all DNA replicated, favourable environment
  • metaphase to anaphase checkpoint: trigger anaphase and proceed to cytokinesis. checks chromosomes attached to spindle
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6
Q

3 negative feedback loops affecting GH and skeletal growth

A
  • somatostatin inhibits GH, GH activates somatostatin
  • GHRH activates GH, GH inhibits GHRH
  • circulating IGF-1 inhibits GH
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7
Q

how does GH cause skeletal growth

A
  • stimulates liver to produce IGF-1
  • circulating IGF-1 reaches bone and drives proliferation
  • local IGF-1 synthesis drives bone proliferation
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8
Q

what do IGF, GH and GHRH stand for and where are they released

A
  • Growth hormone releasing hormone. hypothalamus, with somatostatin
  • Growth hormone. pituitary gland
  • Insulin like growth factor. liver and local tissue (muscle etc)
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9
Q

organ with poor sense of its size and experiment

A
  • pancreas
  • transgenic mouse is generated that expressed diphtheria toxin under control of tetracycline - genetic ablation, kills cells of interest
  • pancreas reduced to 36% of its normal size and only recovered to 40-50% of its normal size
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10
Q

organ with good sense of its own size and experiment

A
  • liver
  • transgenic mouse is generated that expressed diphtheria toxin under control of tetracycline - genetic ablation, kills cells of interest
  • liver reduced to 33% of its normal size and regenerated to 86%
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11
Q

regulation of organ size by TOR pathway

A
  • activates cell growth which increases cell size
  • cell hypertrophy
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12
Q

regulation of organ size by hippo pathway

A
  • hippo inhibits cell proliferation, which would have activated cell proliferation, which would have activated cell number
  • hippo activates cell death which inhibits cell number
  • so hippo shrinks tissue - mutations cause overgrowing/tumours
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13
Q

apoptosis

A
  • deliberate suicide
  • careful coordination of cell shut down, followed by engulfment of remnants by other cells
  • caused by stresses like starvation or DNA damage
  • used development for unneeded cells (eg webbing between fingers)
  • in adult tissue, mainly used for homeostasis (mammary gland-breast shrinks back after breastfeeding) and health (get rid of virally infected cells or genetically compromised tumour cells)
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14
Q

necrosis

A
  • cause by injury, infection, cancer, infarction, inflammation
  • disorderly dying off, w/o signalling to neighbouring cells
  • cells split open and empty contents into surrounding tissue - dangerous, bacteria can start feeding on nutrients
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15
Q

effects of myostatin

A
  • activates Rb, which inhibits proliferation of myoblasts
  • inhibits MyoD which would activate transition from myoblasts to multinucleate myotube
  • secreted by muscle fiber - negative feedback on muscle growth
  • mutations in myostatin cause increased muscle growth
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16
Q

cartilage to bone

A
  • chondrocytes secrete cartilage matrix in the shape of the skeleton
  • over time bone is formed on the cartilage matrix by osteoblasts (ossification)
  • during ossification chondrocytes die by apoptosis
  • cartilage remains in joint areas as adult - shock absorber
17
Q

how to look at skeleton vs cartilage in an embryo

A
  • bone matrix is red when treated with alizarin red
  • cartilage matrix is blue when treated with alcian blue
18
Q

postnatal growth in long bones

A
  • long bones while growing have cartilage on either end and bone forms on the long part (in middle)
  • ossification centers inside joints where bone is forming
  • growth plates between cartilage and bone drive growth: contain chondrocytes that proliferate, hypertrophy and then die, remaining cartilage matrix turned into bone by osteoblasts
  • growth plates close when you stop growing
19
Q

examples of long bones

A

clavicle, humerus, radius, ulna, metacarpus, phalanges, femur, tibia, fibula, metatarsus, phalanges

20
Q

sex specific differences

A
  • girls have earlier growth spurt
  • in embryo, high levels of androgens in ring finger (4D) promote growth
  • high levels of oestrogens in ring finger (4D) repress growth